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UNITED STATES OF AMERICA. 



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DIFFERENTIAL DIAGNOSIS 



CLINICAL MEMORANDA 



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INTRODUCTION TO 
THE OUTLINES OF THE PRINCIPLES 

OF 

DIFFERENTIAL DIAGNOSIS 

WITH 

CLINICAL MEMORANDA 



f by 

Fred. J. SMITH, M.A., M.D. Oxon., F.R.C.P. Lond. 

PHYSICIAN (WITH CARE OF OUT-PATIENTS) AND SENIOR PATHOLOGIST 
TO THE LONDON HOSPITAL 



Wefa fork 
THE MACMILLAN COMPANY 

LONDON: MACMILLAN & CO., Ltd. 
1899 

All rights reserved 
'VI 



OEUVEKfo 



AUG 301809 






40913 

Copyright, 1899, 
By THE MACMILLAN COMPANY. 




•ECOND OOPY, 



Nortooofc ^3«sb 

J. S. Cushing & Co. — Berwick & Smith 

Norwood Man. U.S.A. 



M^t^ OivJlM, V <3. ^ 



PREFACE 

The number of works on medicine, and its various quasi-special 
branches, that claim the time and attention of over-burdened 
students and practitioners is so great that only one excuse should 
be offered for adding to it, viz. either to say something new or to 
put forward a more rational and simpler arrangement of what is old. 
Very little that is new will be found in the following pages, but 
I claim that I have attempted to arrange the old, old phenomena 
of disease in such a manner as to show more clearly their funda- 
mental meanings and relationships. I have utilised the data of 
physiology, and the facts of pathological anatomy, as the source 
^om which to draw inferences and deductions, which in their turn 
constitute a critical analysis of clinical symptoms ; I have endeavoured 
by this analysis to lead up to the underlying principles which govern 
disease as well as health. Once these principles, which are few in 
number, are recognised, bedside symptoms become merely illustra- 
tions of them, varied, it may be, by local and individual peculiari- 
ties, yet ever stamped with such a likeness that the simplest 
induction will speedily explain the organ of their origin. Isolated, 
or apparently isolated, facts thus lose their isolation, and become 
members of a related community ; they no longer require separate 
efforts of memory for their retention, but fall naturally into their 
places as deductions from a universal law. 



vi DIFFERENTIAL DIAGNOSIS 

I thus hope that what I have written will serve not as a text- 
book of medicine, or, indeed, as a storehouse of facts, but as a 
series of pegs whereon to hang a chain of knowledge which will be 
ever increasing link by link as experience grows more ripe, and a 
larger and larger number of varieties of symptoms are recognised as 
varieties, and not elevated to the rank of species by ignorance of 
the connecting links. 

Inasmuch as there is little here that is new, I have mentioned 
very few authorities for the clinical points I have utilised ; they are 
the common possession of the medical profession at large. A few 
original ideas of my own are scattered throughout the work ; time 
and clinical testing alone can show their value, but they are at least 
founded on some considerable experience, and the method of their 
exposition is that which I have found useful in teaching by the bed- 
side. My great wish has been to be as accurate as possible, so as 
not to mislead by false statements, and so sin by commission ; the 
omissions are only too glaring, but limitation of space forbade 
further inclusions. 

FRED. J. SMITH. 
138 Harley Street, W. 



CONTENTS 



CHAPTER I 

Introduction — Definition of diagnosis : Steps in diagnosis — Antitoxin 
treatment — Causes of disease : Comments on the various classes of 
causes — Processes of disease : Inflammation ; Degeneration ; New- 
growths ........ 



CHAPTER II 

Physical signs v. symptoms — Pathology, meanings of — Contagion v. in- 
fection ........ 



CHAPTER III 

Micro-organisms and disease — Reasons for believing a disease to be due to 
microbes — Differential diagnosis of exanthems : General explanation 
of the phenomena ; Special diagnostic points — Varicella v. Variola 
— Variola v. syphilis — Diphtheria v. ulcerated throat— Measles, " 
rotheln, and scarlet fever — Typhus v. typhoid — Cholera v. diarrhoea 
— Erythema — Influenza — Venereal diseases . . .25 



CHAPTER IV 

Diseases of thoracic organs — Section I. Lungs and pleura — Pyrexia — 
Cough, useless and useful — Sputum, quantity, quality — Respiration 



DIFFERENTIAL DIAGNOSIS 

PACE 

— Dyspnoea — Pressure effects— Pain in chest, secondary or idio- 
pathic — Physical signs — Comparison of two sides: Inspection; 
Palpation ; Percussion ; Auscultation — Laryngeal affections — 
Pneumothorax : Cavities — Phthisis, pneumonic, fibroid, hsemor- 
rhagic, miliary, diagnosis of — Pneumonia, incipient, central ; Is 

it a specific disease ? — Acute bronchitis and bronchopneumonia 

Chronic bronchitis, its pulmonary complications — Pleurisy, causes 

of— Pleuritic effusion — Intrathoracic growths — Growth v. aneurysm . 47 



CHAPTER TV— Continued 

Section II. Heart and pericardium— Local symptoms and physical signs 
— General symptoms and physical signs — Heart organs: Hyper- 
trophy and dilatation ; Compensation and failure ; Diagnosis of 
hypertrophy and dilatation, of compensation and failure — Endocardial 
v. exocardial sounds— Indications and meaning of bruits— Morbus 
cordis without bruits — Ulcerative endocarditis : Its pathology and 
diagnosis : Prognosis in heart disease 



CHAPTER V 

Diseases of nose, throat, and alimentary system— Haemorrhage : From 
nose, causes ; Issuing by mouth, local causes— Haematemesis v. 
haemoptysis : Causes of haemoptysis ; Causes of haematemesis— 
Issuing by anus— Causes of melaena— Causes of haemorrhage per 
anum— Vomiting : Causes— Colic : Diagnosis of causes of ; Treat- 
ment of— Colic without collapse : Differential diagnosis of causes of 

— Colic v. peritonitis— Differential diagnosis of forms of calculus 

Diarrhoea and constipation, causes and diagnosis of— Diarrhoea in 

phthisis — Ascites, primary groups of— Ascites v. encysted fluid 

Dyspepsia v. gastric ulcer ..... I4 g 



CHAPTER VI 

Diseases of the urinary organs— Normal urine, variations in health ; 
Variations in disease, frequency, quantity, colour, specific gravity, 

pathological constituents, tests for and meaning of— Albuminuria 

Surgical kidney— Pyuria, causes and diagnosis of— Haematuria, 
indications of locality and cause— Casts— Urates— Oxalates— Phos- 



CONTENTS ix 

PAGE 

phates — Uric acid, consideration of — Sugar, consideration of — 
Uraemia, diagnosis of — Suppression v. retention : Causes of suppres- 
sion and retention — Bright's disease, varieties of — Urine in consecu- 
tive nephritis — Stone, tubercle, and carcinoma of kidney — Diabetes, 
phosphatic, insipidus . . . . . .185 



CHAPTER VII 

Affections of joints — Symptoms of joint trouble — History of illness, etc. 
— Charcot's joints — Flat foot — Gonorrhceal rheumatism — Gonorrhceal 
rheumatism v. simple — Traumatism — Hysteria — Synovitis — Tubercle 
— Rheumatism — Gout — Rheumatic gout — Rheumatoid arthritis — 
Differential diagnosis of last four affections — Arthritic diathesis . 229 



CHAPTER VIII 

Section I. Anatomy and physiology of the nervous system — The neuron 
— The peripheral nerves — The cord — Medulla — Brain— Functions of 
the same — Motor, sensory, and reflex tracts — Trophic influences — 
Inco-ordination — Section II. Table of diseases of the nervous system 
— Section III. Differential diagnosis of nervous diseases — Essential 
v. secondary ; Organic v. functional — Peripheral neuritis — Spinal 
cord, systems of, indiscriminate lesions of — Cord v. peripheral nerves 
— Medulla and pons, tracts and cells in — Mid-brain hemiplegia — 
Cranial nerves — Brain — Jacksonian epilepsy — Traumatism — Organic 
lesion — Tumours of brain . . . . . .247 



CHAPTER IX 

Urgency cases — Haemorrhage — Other vascular lesions — Traumatism — 
Sudden death — Lesions of nervous system — Poisoning — Differential 
diagnosis ........ 326 



CHAPTER I 

INTRODUCTORY REMARKS ON DIAGNOSIS IN GENERAL 

Dr. Pye Smith once denned pathology very pithily as "a chat 
about the etiology of disease." Though I think the definition some- 
what too narrow, we may accept it provisionally and then define 
diagnosis as "the complete analysis of etiology," for we cannot 
consider a diagnosis as absolutely final and finished until we have 
probed etiology to the bottom. The process of diagnosis, thus 
scientifically considered, will then consist of three stages : — (i) The 
collecting of as complete a list as possible of the immediate pheno- 
mena of disease which are universally and by common consent 
termed symptoms and physical signs, e.g. cough, pain, diarrhoea, 
paralysis, palpitation, etc. (2) Inferring or deducing from these 
collective phenomena a primary or gross diagnosis as to the organ 
or organs affected and the general nature of the disease, e.g. bron- 
chitis, dyspepsia, neuritis, morbus cordis, etc., thus arriving at what 
we may call the generic title of the affection. (3) A final step, 
viz. the identification of the specific cause at work, thus adding a 
specific name to the generic one, e.g. tubercular bronchitis, gouty 
dyspepsia, septic pneumonia, rheumatic arthritis. 

The first of these three steps is naturally the simplest proceed- 
ing, for it consists only in taking a complete history of the case. 
Each hospital school has its own particular method of case-taking, 
and each teacher naturally thinks his own school the best, and I 
therefore give a preference to the following card, which is in use at 
the London Hospital. It has, I believe, at least the merit of not 
omitting anything of importance if used systematically. 

e b 



DIFFERENTIAL DIAGNOSIS chap. 

Instructions for case-taking in Medical Wards : — 
I. The Clinical Clerk to enter the heads of the case, and date of 
the Patient's entry to Hospital, and fill in the registered 
number as soon as possible. Insert dates at which the notes 
are taken. 
II. State what the patient complains of — using his or her own words 
verbatim as far as possible, and when using the names of the 
days of the week, be sure to insert also the day of the month. 
III. Family History — Number and condition of health of those 
living. Ages and diseases of those dead. Note any family 
tendency to disease. 

This section is especially useful for the following diseases — 
rheumatism, gout, phthisis, haemophilia, nervous diseases, 
asthma, heart disease ; though it must not be omitted in 
any case. 

Personal History — Habits (stating quantity and kind of 
alcohol taken), occupations, residences, previous diseases 
and illnesses, noting especially the dates of illnesses or 
changes. If in Hospital before, get the registered number, 
and insert it in the present notes. Especially, never 
omit to inquire for any disease which may stand in etio- 
logical relationship with the present illness, e.g. rheumatism 
with tonsillitis or morbus cordis, gout and lead poisoning 
with cirrhotic kidney, syphilis with many conditions ; these 
three diseases should never be omitted, their absence, as 
well as presence, being equally carefully noted. 

Present Hlness — Date and manner of commencement : order 
of symptoms and dates of occurrence. A useful question 
here is — When were you last quite well ? and trace the ill- 
ness step by step from this. 

Probable Cause — Insert here your own opinion and also that 
of your patient, and any higher available opinion. 

IV. Present Condition — General condition. This should never be 
omitted ; the most important items are perhaps — expression 
of face, colour of face (anaemia, cyanosis, etc.), oedema, 
nutrition, distension of veins, sleep, easy respiration, etc. ; 
note position of patient in bed, whether sitting up or lying 
down, whether restless or comfortable and quiet, etc. 
V. Digestion — Tongue, teeth, throat, appetite, vomiting, haemate- 
mesis, bowels. 

Symptoms — Fulness or pain after food, flatulence, colic or 
other disturbance. Abdominal pain or tenderness. 



I DIAGNOSIS IN GENERAL 3 

Liver — Size and character as determined on percussion and 
palpation. Whether tender or not. Jaundice. 

Spleen — Percussion, palpation. 

Abdomen — Its physical condition as indicated by palpation, 
percussion and mensuration. Distension, retraction. 
Ascites. Tumour. Abdominal pain. 

VI. Vascular System — Pulse frequency and characters, condition of 
arteries, veins, capillaries. Heart palpate, percuss, auscultate. 

Symptoms — Palpitation, precordial dulness, pain, etc. 

VII. Respiratory System — Dyspnoea, frequency, characters of respir- 
atory movements. Cough, expectoration, haemoptysis. 

Physical examination, inspection, palpation, percussion, auscul- 
tation, condition of larynx. 

VIII. Nervous System — General condition. Intelligence, mental 
state, sleep, speech. Vertigo, delirium, coma. Complaints 
of head pain, vomiting, numbness, neuralgia. Paralysis, 
convulsions, spasms, tremor. 

Motor power— Limbs, trunk, action of sphincters. Ability to 
walk and do ordinary work. Power over large joints, 
small joints, finer movements of fingers, e.g. writing. 

Cranial nerves — Movements of eyes, tongue, face, palate. 
State of pupils. 

Special senses — Ophthalmoscopic appearances. This should 
never be omitted, but is more especially important in (1) 
anaemia, (2) Bright's disease, (3) cerebral and spinal 
diseases, (4) syphilis, (5) any disease in which amblyopia is 
complained of. 

Sensibility — Tactile sensibility of skin, anaesthesia, hyper- 
esthesia, dysesthesia (perverted sensations, e.g. numbness, 
burning pain, etc.). Sensibility to heat and cold. 

Reflexes — Superficial and deep. Patellar, plantar, wrist, ab- 
dominal, cremasteric, etc. 

In Spinal Cases, gait in walking, power in each limb, condition 

of sphincters. 
In any nervous case the special points to be attended to 

without exception in any case are (1) hereditary, (2) manner 

and time of onset, (3) condition of reflexes, (4) static and 

locomotor equilibration. 



4 DIFFERENTIAL DIAGNOSIS chap. 

IX. Locomotor System — State of bones, muscles, joints, scars, 
nodes. Skin, moist or dry. Bed sores. 

X. Lymphatic Glands — Neck, groins, axilla. Size, mobility, sup- 
puration. 

XI. Urine — Frequency of micturition. Quantity, colour, reaction, 
specific gravity. Albumen. Sugar. Deposit. Microscopical 
and chemical characters of deposit. 

XII. Generative System — Menstruation, frequency, duration, quan- 
tity in excess or otherwise, whether painful, other discharges. 
Conditions of uterus and pelvic organs (when examination is 
possible). 

XIII. Treatment — Prescriptions and diet to be entered, and all alter- 

ations noted with dates. 

XIV. Progress of Case to be noted as occasions may require. Pulse 

should be recorded whenever the temperature is taken. Urine 
must be noted at least once a week. 

When important symptoms or complications occur, besides a 
description in the text, an indication should be given in the 
margin. As a good general hint for note making, remember 
in all cases, without exception, a note should be made on 
the first day after admission ; in all acute cases a note 
should be made every day while the symptoms persist; after 
this, notes may be made less frequently, but any fresh symp- 
tom or complication must be immediately noted. 

XV. Result — A description of the patient at the time of discharge, 
or the mode of death, should be given at the termination of the 
case. This is, in some respects, the most important part of a 
Clerk's duty, and must on no account ever be omitted in any 
case. The description need only be of that system or systems 
which have been affected by the disease. 

The C/im'cal Clerk to sign his name in full on completion of 
the case. 

At the second step diagnosis frequently stops short ; possibly, 
though let us hope rarely, from carelessness or indifference on the 
part of the observer, as when a cough or diarrhoea is treated by a 
dose of opium (reluctance on the part of the patient to submit 
himself to thorough examination has sometimes too to be over- 
come) ; more frequently and excusably because further information 
is useless in the present state of our therapeutical knowledge, or 
because some very obtrusive symptom must be immediately subdued 



I f DIAGNOSIS IN GENERAL 5 

if the patient's life is to be saved even temporarily, as may happen 
in hyperpyrexia from any cause, or in the agony of calculous colic ; 
most frequently and really unavoidably because the further informa- 
tion required is absolutely unattainable until death has afforded the 
opportunity for more thorough investigation, as in a case of severe 
haemoptysis, for example, or rapidly fatal septic pneumonia or per- 
forative peritonitis. Like the first step, this second one is in many 
cases a very simple matter, but to the student and young prac- 
titioners it is apt to appear easier than it really is. Nothing but 
wide experience by the bedside and, above all, in the post-mortem 
room, will convince us of the difficulties which surround even the 
simplest accurate diagnosis, and there can be no greater mistake 
than that of at once accepting the most obvious as the most correct. 
Apart from the above exceptions and difficulties, it should always 
be our endeavour to take the third and final step in diagnosis. Of 
its importance generally in clinical medicine examples are almost 
superfluous, the point is so universally admitted. I need only 
mention the flood of light thrown on an obscure case of albuminuria 
by the recollection of a forgotten attack of — it may be mild — scarlet 
fever, what a relief to our anxieties it is to find a bad sore throat as 
a precedent fact in a case of squint, and, per contra, how the dis- 
covery of the bacillus tuberculosis in the sputum redoubles our 
anxieties about what was previously looked upon as a simple 
catarrh. But beyond all this the discoveries of the last quarter of 
a century in bacteriology have made this third step of much greater 
importance still, for they have held out to us hopes of cure in many 
cases hitherto incurable. Whether these hopes are destined in the 
future to be realised or disappointed it would be rash to prophesy, 
though certainly the results hitherto obtained are encouraging. 
As the basis on which these hopes are founded is very germane to 
the completion of a diagnosis, we may here enunciate its principal 
points. Stated in order the argumentative propositions run thus : — 

(1) Many groups of symptoms or diseases are caused by 

microbes invading the body. 

(2) In many of these, if not in all, the actual symptoms are 

caused by a toxin or toxins manufactured by the 
microbes, either directly from their own metabolism or 
indirectly from the tissues of the victim. 

(3) The spontaneous cure of such symptoms is, at least in some 

cases (possibly or probably in all), effected by an anti- 
toxin or neutraliser of the previous toxin; this in turn 



6 DIFFERENTIAL DIAGNOSIS chap. 

may apparently be produced either by the microbes or 
the tissues. 

(4) Such antitoxin can be obtained, with more or less success 

(by methods which need not here be entered upon), in 
quantities and condition available for therapeutic uses. 

(5) It should follow, and has in many cases already been proved to 

follow, that the injection of such antitoxin, if effected early 
enough in the disease, is efficacious in curing the patient. 

These propositions would appear to be scientifically demon- 
strated, but there is one point which is still in doubt, and that the 
most important one from our present point of view; it is this — 
does each separate and identifiable microbe produce a special and 
specific toxin, i.e. a poison of definite composition — as definite, say, 
as morphine or other alkaloid — peculiar to itself and requiring for 
its neutralisation an equally definite and specific antitoxin? or, on 
the other hand, do many different microbes produce a common 
toxin, so that the antitoxin produced by one microbe or method of 
preparation can be used for the toxin of another kind of microbe? 
All the evidence — at least the weight of evidence — we at present 
possess points in the direction of the former of these two supposi- 
tions being the true one. Witness the almost conclusive clinical 
experience in the treatment of diphtheria, of rabies, and of tetanus, 
as well as the brilliant successes and the disappointing failures in 
cases of septic disease, in which the particular microbe at work is 
less definite or less familiar, and where success has been com- 
pulsorily attributed to the right antitoxin, failure being due either 
to the wrong antitoxin or to a too late application. I think, there- 
fore, we shall be obliged ultimately to admit its truth, and we can 
see at once on this admission how enormous is the importance of 
the third step in diagnosis, to be able to say, " This case of illness 
is due to this particular microbe, and I must use its antitoxin as 
quickly as possible." 

Besides this therapeutical use of a completed diagnosis, the 
principle of toxins and antitoxins has lately been applied to that 
completion itself, vide Typhoid Fever. May we not hope in the 
future to see the two procedures more frequently working hand 
in hand, complementary to one another? 

Causes of Disease in General 

In the special sections of this work we shall always be consider- 
ing diagnosis as an induction from symptoms. We may here in the 



i DIAGNOSIS IN GENERAL 7 

introductory or general chapter briefly review the matter from the 
other standpoint, and see what are the causes of disease and the 
general processes by which these causes produce the symptoms 
which we have later to analyse. 

The fundamental causes of disease belong to but few really 
separate categories, which may be presented in comprehensive 
forms as follows : — 

Causes of Disease 
A. From without (environment in the larger sense) : — 



■5 s> 



(Chemical (on the surface of the body). 
Grossly physical effects, and those of excess of heat 
and cold 

lice, 
-! bugs, etc. 
[internal — worms, etc. 
'(1) Essentially patho- 
genic, or (2) rend- 
ered so by peculiar 
opportunities of vital- 
ity or food supply. 

arsenic, alkaloids, pto- 



Parasitic 



Poisons 



, , . , , I External — fleas. 

Macroscopical or coarsely ) 

microscopic 



Finely microscopic (mi- 
crobes) 



■5 s d 2 

O 3 






o % 

Mi u 
O © 

be -S 



Recognised as such 
maines, etc. 

Ordinary articles of food rendered injurious by 
circumstances of too free indulgence, imperfect 
mastication, decomposition, etc., and also by 
unusual changes in digestion with absorption of 
poisonous ptomaines, etc. 

Perforation of a hollow tube from any cause what- 
ever. 

Direct extension of processes of disease from one 
organ to another. 

Carried in the blood or lymph stream, convected 
from place to place. 

Forced malpositions, as twisting of tubes and dis- 
locations of more solid organs. 



B From within (idiopathic, so to speak) 



{a) The more or less direct effect of altered function in 
one organ upon another organ, e.g. the inter- 



8 DIFFERENTIAL DIAGNOSIS chap. 

related functions of liver, stomach, kidney, 
pancreas, etc. 
b) The effects of wear and tear, age in its physiological 
sense. 

(c) Congenital or inherent debility of tissue either 

absolute or relative to the work demanded of it. 

(d) New growths of intrinsic formation. 

That the apparently innumerable causes of disease should be 
reducible to such a small number of independent types is at first 
somewhat startling, but I think a little consideration and comment 
will show that the above errs on the side of excess rather than 
defect, and that some of the groups overlap. 

Traumatism. — In its widest sense — of injury — this would in- 
clude nearly all the other causes of ill health which arise from the 
environment of the individual. Food imperfectly masticated or 
otherwise by its physical qualities unsuitable for digestion is, for 
example, very likely to cause a wound of the stomach with its 
attendant evil consequences. In its grosser sense the cause belongs 
almost entirely to surgery. We may recognise its probable single 
action when health speedily returns after the removal of an exciting 
causa causans. Mr. Hutchinson would refer most skin diseases to 
this category or the next. 

Parasites. — Of the grosser forms of external parasites the action 
is mildly irritative or traumatic, increased largely by scratching or 
rubbing. If through the wounds thus produced microbes find an 
entry to the blood or lymphatic vessels — the skin teams with ever 
watchful enemies of this character — the result may be as bad as, 
in fact is identical with, the other microparasitic troubles, the skin, 
instead of some mucous or other surface, being the point of 
entry which is thus more easily traceable. Of the larger internal 
parasites — collectively denominated worms — the results are more 
varied. Thus round and tape worms may reside within us without 
causing any trouble whatever, but they may cause much irritation 
with reflex symptoms, they may block passages, e.g. the common 
or cystic bile duct, or cause tumours (hydatids), or by migration of 
the young {Trichina spiralis) cause serious symptoms in any organ ; 
the Anchylostoma duodenale may produce profound anaemia by 
abstraction of blood. 

To the second — finely microscopic — group of parasites the ever- 
multiplying discoveries of medical science are rapidly relegating 
every disease to which human flesh is heir. Possibly enthusiasm 



I DIAGNOSIS IN GENERAL 9 

rather than hard facts is having something to say in this matter. 
When present in numbers, or with virulence sufficient to create a 
pathological disturbance in the body, they have one almost invari- 
able and common result, viz. pyrexia (in primary syphilis, in gonor- 
rhoea, and possibly a few others — chronic rheumatoid arthritis, for 
example — this is least marked, and even in tubercle it is doubtful 
how much of the fever is due to the specific bacillus), a result to 
be expected when we consider the enormously preponderating influ- 
ence which metabolism has in the production of our supply of body 
heat, and then remember that in microbic disease either a toxin or 
a contagium vivum is, or may be, carried all over the body, stimu- 
lating every part of it to a metabolic antagonism. 1 This pyrexia 
itself, however, almost immediately offers points of difference aiding 
diagnosis, in suddenness of onset and rise, in duration, in irregular 
variability or regular periodicity; cf. typhoid and typhus, scarlet 
fever and measles, malaria and general septicaemia, etc. In many 
cases, too, the seat of inoculation or of first morbid appearances is 
available, the uterus in the puerperium, the tonsil in diphtheria, the 
genito-urinary apparatus in venereal diseases. Still later we have 
the selective seat in which the poison has left its traces, such as the 
peripheral nerves in diphtheria, the kidneys in scarlet fever, the spleen 
in malaria, etc. Further points will be found in the special sections. 
Poisons. — Poisons, as ordinarily understood, may be divided 
into three classes : (1) Those which act upon the alimentary canal, 
and are practically not absorbed, e.g. all corrosives and many 
irritants; (2) those which only act after absorption, e.g. most alka- 
loids ; (3) those which act in both ways typically, phosphorus, 
arsenic, and oxalic acid. The first and last classes will show ali- 
mentary symptoms in excess, vomiting and diarrhoea within a short 
time of being taken, and have one point in common, in marked 
contrast to the common symptom in microbic invasion : this is 
a subnormal temperature, largely induced by shock and mental 
anxiety. The second class in its entirety, and the third in the 
later phases of a case, show appropriate features according to the 
selective affinity of the poison for special organs, digitalis for the 
heart, conium and strychnine for the motor nerves, phosphorus 
for liver and muscles, opium and belladonna for the cerebral cortex, 
etc., and thus the case may be provisionally or even finally diagnosed 
in conjunction with the history. 

l This metabolic activity or antagonism not only explains the phenomenon of 
pyrexia, but also lies very close to the root of what {.vide Processes of Disease) we 
know as inflammation. 



io DIFFERENTIAL DIAGNOSIS chap. 

When articles of diet become injurious, they too, like the more 
virulent poisons, produce symptoms in one of two ways: (i) by 
acting as immediate irritants to the alimentary canal, with vomiting 
and purging, as in ptomaine poisoning, or in actual surfeit of food 
otherwise wholesome; (2) by pouring into the blood or lymph 
stream a greater supply of nutriment than can be adequately 
disposed of in the great chemical laboratories of the body ; hence 
arise, more immediately, unpleasant sensations in the shape of 
sleepiness, biliousness, headache, etc., and remotely, a storing up 
of an undue amount of fat — obesity — flabbiness of body and mind, 
general lassitude, etc., and perhaps more remotely still, gout and 
goutiness, with all their pains and penalties, and possibly also a 
lessened resistance to attacks of microbic troubles. 

Immediate Surroundings. — From the little world of its own 
special environment every internal organ, which has no immediate 
and direct communication with the larger external world, gets all 
its serious troubles. The blood and lymph that bathe its tissues 
bring with them the chemical or vital poisons that interfere with its 
physiology, or cause grosser mischief still, e.g. nephritis, acute 
yellow atrophy, meningitis, endocarditis, etc. ; the perforation of a 
tube allows its contents to become a serious source of irritation to 
neighbouring structures — gangrenous inflammation from extra- 
vasation of urine, for instance, when ureter, bladder, or urethra is 
ruptured, or peritonitis when the contents of the alimentary canal 
are allowed to escape freely into the peritoneal cavity. Inflamma- 
tion has but slight respect for the fascial or fibrous boundaries 
laid down for its guidance by anatomists, but spreads with but little 
hesitation from meninges to brain or cord, from endo- or peri- 
cardium to myocardium, from stomach to liver, etc. Displacements 
of the heart by pleural effusions or more solid growths will cause 
serious interference with the circulation ; a displaced kidney brings 
about a great deal more than simple mental worry ; twisting of the 
gut, or even of a pedicelled tumour, may, and often does, bring about 
a fatal illness. All these are illustrations of the working of the 
internal environment, and yet there are but few of them which 
with equal propriety might not be put under the heading primarily 
of poisons or traumatism. 

Arising from within — Idiopathic Diseases. — It is only by 
courtesy — because we cannot always discover the original culprit — 
that disease in one organ, almost certainly arising from the wrong- 
doing of another, can be called idiopathic, or that this group can 
retain its position amongst the primary causes of disease. We often 



i DIAGNOSIS IN GENERAL n 

speak of a primary congestion of the liver, or of an idiopathic 
anaemia, but in both cases it is extremely probable that the ali- 
mentary canal is the first offender by passing an excess of suitable, 
or some unsuitable, material to the liver or blood, which in turn 
exhibit the symptoms of complaint ; and even now we have to throw 
the blame rather on the individual, who has by over-feeding or 
neglect of defalcation originally induced a plethora of nutrient 
material or absorption of poisonous products of food decomposition 
unavailable for nutritive purposes. In pneumonia and bronchitis 
danger but rarely arises from obvious asphyxia ; it is almost constantly 
due to the difficulties the heart experiences in keeping up the circula- 
tion. This in turn may be due to the imperfect oxygenation of the 
blood by the lungs. Still the lung trouble is originally derived from 
without. When the functions of the kidney are imperfectly per- 
formed every organ in the body feels it, owing to imperfect removal 
of waste ; yet the kidney itself has suffered for the fault of 
stomach, or from the introduction of microbic toxins. In fact, the 
more we inquire into this group of causes, the less the reason for 
retaining it, and the more does it divide itself up amongst the other 
groups. 

Wear and Tear. — In wear and tear we get the first trace of 
disease really independent of external conditions ; they are the 
essential conditions under which all living things exist. It is a 
common idea with the laity that in seven years every cell of the 
body is changed in its constituent molecules. As far as I know, 
there can be no exact foundation for this belief, but it probably, 
for all that, contains a pregnant approximation to the truth, and 
should loss — however gradual — be not equalled by repair and re- 
placement, function must suffer, with the inevitable reaction known 
as dis-ease. The deficit in childhood is evidently nil, and as age 
advances, with waning elasticity in power of repair, it may be 
extremely minute, so that many years may elapse before the 
resultant loss of function is sufficient to attract attention. I think 
it probable that many cases of so-called cirrhotic kidney — and a 
better illustration of a chronic insidious disease could not be given 
— are thus induced. The kidney mischief — want of repair in 
epithelial cells — acts and reacts in turn upon the vascular system, 
where indeed, in the shape of arterio-capillary fibrosis and atheroma, 
the effects of age are more visible and pronounced, and also more 
serious than in any other organ or tissue. This vascular degenera- 
tion operates in two ways: (i) directly, the vessels themselves 
becoming brittle and absolute rupture taking place, or by losing 



12 DIFFERENTIAL DIAGNOSIS chap. 

natural elasticity x they gradually yield to the blood pressure within 
them, and aneurysms, large or small, single or multiple, form, with 
all their attendant dangers; (2) indirectly ; the minuter vessels by 
their pathological changes either (thrombosis) starve outright the 
tissues to which they are distributed, or (by thickening and altera- 
tion of wall) interfere with that due interchange of nutrient and 
waste material which is the life of the tissues, and thus lead to 
such impaired vitality that the tissues cannot adequately resist 
untoward influences — toxins, etc. — nor properly repair damage 
inflicted upon them. It is by such considerations as these' that 
we are led easily to understand how in old people or those prema- 
turely worn out (alcoholic excesses, physical toil, chronic lack of 
nourishing food) the prognosis of disease is made much worse, 
and also to appreciate why symptoms in such patients may be 
unexpectedly obscure or insidiously vague ; pyrexia, that constant 
accompaniment of metabolic resistance and cell warfare, may be 
but slight, or even absent in cases which would otherwise be termed 
acute ; the foundations of life may be sapped and death intervene 
while we are still waiting for the explosion of general and local 
manifestations that should tell us where the enemy is attacking ; 
a smouldering pneumonia, an apyrexial empyema, a chronic and 
insidious uraemia will illustrate the point. 

Congenital op Inherent Debility of Tissue. — Considered strictly, 
this whole group can only be a particular illustration of the influence 
of the immediate environment, of the physiological — or pathological 
rather — influence of one organ upon another, for during intra- 
uterine life the fcetus is as much a part of the mother as her kidneys 
or heart, and is as much dependent for its health and integrity 
upon the due interrelation of her organs as are those organs them- 
selves dependent upon one another. For more practical or clinical 
purposes, however, the matter assumes a different aspect, and we 
may divide these into three fairly distinct categories. First, those 
cases in which an active process of disease is going on in the child 
at the time of birth, a disease which has actually attacked it — been 
transmitted to it conveys a slightly different impression — while it 
was part of the mother. Syphilis and the acute specific fevers offer 
us typical examples of this, and recent reports w r ould seem to 
render it possible, if not probable, that tubercle may in a similar 
w r ay attack a child in utero. Simple anatomical deformities might 

1 It must be remembered that elasticity essentially consists in a " power to return 
to an original form after a distorting force of any kind — pull, pressure, or twist — has 
ceased to act." 



i DIAGNOSIS IN GENERAL 13 

be placed in the same class. Secondly, those cases in which 
inherent defect of tissue is assumed — rather than proved — to exist 
to explain certain so-called idiopathic affections. A child, for 
instance, is born healthy to all appearance, and remains so for years, 
and yet without any ascertainable cause disease makes its appear- 
ance in certain structures or organs ; mental deficiencies, primary 
sclerosis of parts of the nervous system, primary myopathies, haemo- 
philia, would be examples of this class, amongst many others, in 
which we invoke heredity as a deus ex machina. Thirdly, the prin- 
ciple may with a little extension be used to explain those delightful 
words, "idiosyncrasy," "dyscrasia," "diathesis," etc., which are such 
beautifully simple ways of explaining (! !) our ignorance of etiology. 
Thus, a number of people take a similar dose of a drug ; some 
exhibit marked effects, others none. Why ? Oh, idiosyncrasy ! 
Again, a dozen individuals are exposed to the same unusual dis- 
turbance of gross environment ; one gets acute rheumatism, another 
nephritis, another pneumonia, another pleurisy, another chorea, 
and some show no trace of the storm. Why? Oh, different 
diatheses is the glib reply. However, explain or mystify the matter 
as we may, the facts remain, and we utilise them clinically when we 
insist upon the importance of careful inquiry into the family history 
of a patient, and into the previous illnesses that may have occurred 
of a similar nature to that for which our advice is sought. The 
layman puts the same idea into different words when he exclaims, 
" The old doctor is the man for me; he understands my constitution." 
New Growths. — Of the exact etiological factors underlying the 
starting of a primary new growth, our real knowledge up to now 
amounts to — nil. Pathologists were lately — and perhaps even 
now are — keen in the pursuit of a hypothetical cancer microbe — 
a psorosperm, it was called. If such exists, its entrance, its life, and 
its death are still mysteries to us. The only clinical causes we can 
yet appreciate are blows as the starting-point of many sarcomata, 
and chronic irritation for many epitheliomata, but we still await 
anything like an explanation of the vast bulk of growths of a 
malignant — or innocent, for that matter — nature. Cohnheim's 
theory of fcetal remnants is perhaps as fascinating as any ; but 
even this goes but a little way. 

Processes of Disease 

However few the really independent causes of disease are thus 
seen to be, the individual morbid processes which they excite are 



i 4 DIFFERENTIAL DIAGNOSIS chap. 

still fewer, for they overlap one another even more than the causes, 
both in their intermediate phases and in their final results. Of 
intermediate phases only two are possible. Every organ and tissue 
in the body possesses two primary attributes — structure and function, 
— and the processes of disease can only exhibit themselves as inter- 
ferences with one or the other, or more probably with both, of these 
attributes ; the diagnosis and discrimination of these interferences 
constitute the whole of our morbid anatomy and physiology. With 
microscope and naked eye we attempt, after death, or in fragments 
removed from the living, to find and to study the alterations in 
structure, and with the clinical eye we endeavour to penetrate the 
mysteries of altered function. Our instruments of sight, natural 
and artificial, aided even by most elaborate staining processes, are 
very imperfect for studying the finer — molecular ? — structural 
changes, and hence, though much has been revealed, very much 
more remains to be discovered. But the omissions are the less 
important from a clinician's point of view, because, firstly, we 
cannot be sure that what is seen was there during life ; and, 
secondly, because of the limited capability of nature and the still 
more restricted power of drugs to restore structural damage, even 
when it can be detected or surmised. We cannot, moreover, 
determine what is reparable and what is not, except by that means 
which is our only therapeutical hope, viz. by endeavouring to 
promote to the utmost harmonious function, the loss of which is 
indeed but too frequently our only means of guessing that structure 
has suffered. The power, on the other hand, of the clinical eye is 
only limited by the amount and character of the intelligence which 
can, by reading and experience, be brought to bear upon unravelling 
the intricate web and woof of symptoms, upon determining which 
of them are primary and essential, and which are secondary or of 
less moment ; which we can directly influence, and which must be 
left to the control of other organs. 

The gross or comprehensive processes by which these inter- 
ferences with structure and function are brought about are : — 

i. Inflammation. 

2. Degeneration. 

3. New growths. 

Inflammation. — Into the microscopic details of diminished 
drainage from, and excessive entrance of blood and serum into, 
an inflamed area or organ I do not propose here to enter, nor 
into the diapedesis of white and red corpuscles, nor to the differ- 



i DIAGNOSIS IN GENERAL 15 

ence between these cells and pus, nor into the vexed question of 
the origin of fibroblasts. Collectively, all these constitute the struc- 
tural changes which we can see, and the student is too apt to lose 
himself in these details of a microscopic slide and not to think 
of the functio Icesa of vessels and tissue cells which, from the 
medical, as opposed to the surgical, point of view, is the chief, if 
not the only, object that requires attention. It is true that we 
frequently call upon a surgical colleague, and rightly too, to empty 
by artificial means a serous cavity which has become filled with the 
products of inflammation, but it is immaterial to a clinician whether 
the nucleated cells that appear at a focus of inflammation are pro- 
fessional policemen or special constables sworn in for the occasion ; 
it is immaterial whether repair be executed by builders called in 
for the purpose from a distance, or by the inhabitants living in the 
neighbourhood ; they all have to be nourished by the food in the 
blood, they all are worried by similar irritants, and our only concern 
is to remove the irritant as speedily as possible and do our best to 
keep the blood in good condition. 

The functio Icesa of capillary blood-vessels leads to excessive, 
insufficient, or improper food supply to, and imperfect drainage 
from, the special or specific cells of a part ; this leads to altered 
vitality in these cells, and this in turn is exhibited by disturbance in 
their function — excess, perversion, or diminution, — and eventually, 
if the trouble be severe enough or long enough continued, the cells 
die outright. It is thus that we must think of inflammation in its 
earlier active phase — kidney cells treated in this manner allow 
wrong materials, albumen, etc., to escape in the urine ; they fail to 
pass on the right substances, or even cease to secrete at all ; hepatic 
cells cease their glycogenic and bile formation functions, or perform 
them wrongly ; the cells of the alimentary mucous membrane ex- 
crete vitiated digestive fluids, and when digestion has thus been 
improperly performed, absorption becomes a harmful process, the 
gut muscle too is hurried into excessive action, and diarrhoea 
ensues, or, if it be involved seriously in the trouble, its function 
ceases, and paralytic obstruction — the most serious of all forms of 
recoverable obstruction — occurs ; in the lungs excessive secretion 
or effusion fills the air cells, and thus brings about cessation of the 
aerating function ; imperfect nutrition of nerves sends them astray 
in functioning, and their property of irritability becomes excessive, 
insufficient, or perverted, and so the illustrations might proceed 
through the body. 

The functio Icesa of the tissue cells may thus be secondary to 



1 6 DIFFERENTIAL DIAGNOSIS chap. 

that of the capillaries, but more frequently in medical practice we 
see it as a primary phenomenon due to a toxic condition of the 
nourishing plasma which surrounds them ; under these circum- 
stances the cells cease to a large extent their own specific activities 
and take up ones that are foreign to them, manufactory of an anti- 
toxin and other unusual metabolic processes. When thus struggling 
against unnatural conditions they are very liable to be attacked by 
fatal structural changes unless relief be speedily afforded them. It 
is thus I understand the evil effects of the working of blood- 
poisoning, whether this be generalised over the whole body, as in 
zymotics, or whether it arise from some quite localised process, as 
in a poisoned wound with absorption therefrom. 

When these destructive phases of inflammation have ceased and 
nature exhibits her limited power of parenchymatous-cell reproduc- 
tion, we must remember that the new or young cells have to learn 
their business and get accustomed to variations in their environ- 
ment ; they are likely at first to be of feeble vitality and resisting 
power, and chronic exfoliation may thus be kept up till irreparable 
damage is done to the organ of which they form the essential 
constituent. 

And lastly, when repair is complete we have to realise the 
strangling effects of the new-formed fibrous tissue, which, in us, is 
the best that nature can do to fill up a gap. This fibrous tissue 
cannot pick out urea nor biliary constituents from the blood, it 
cannot absorb peptones or fats or oxygen, it cannot transmit 
messages, nor can it contract and relax in response to messages 
received ; it has only one function, that of contraction into a con- 
dition of stable equilibrium, and this it exercises with most per- 
nicious effects on vessels and parenchymatous cells, strangling the 
one and starving the other. 

I have written at some little length on the local processes of 
inflammation in the hope of making it clear that a scar in the 
kidney is identical with one in the lung or liver, that a catarrh of the 
bronchi is identical in its processes with one of the gut ; that, 
in fact, the principles once grasped, details can be evolved with 
readiness for special cases, and pathology thus changed from a 
heterogeneous collection of wearying facts to a splendid illustration 
of fundamental laws working on lines variable within small and 
special limits. 

Degeneration. — In text-books of pathology it is usual to de- 
scribe this process as either a primary or a secondary phenomenon, 
and then to give particulars of many varieties : amyloid, brown, 



i DIAGNOSIS IN GENERAL 17 

glassy, cloudy, fatty, mucoid, colloid, fibroid, etc. Important as 
this knowledge is from many points of view, it may for our present 
purposes be largely ignored, for both forms and all varieties mean 
clinically very much the same thing, viz. diminution in vitality and 
functional capacity, and ultimately death, of the parenchymatous 
cells, whose fate is being discussed. 

The primary form, strictly speaking, has for its underlying 
essence either natural wear and tear, or congenital and inherent 
poor quality of material, both of which have been already alluded 
to as primary causes of disease ; but it is usual in clinical medicine 
to think of and accept as primary many varieties of degeneration, 
fatty, etc., which are in reality induced by an insidious form of chronic 
poisoning or starvation through the blood supply, which in its turn 
is influenced primarily by the alimentary canal and the substances 
put into it and absorbed thence. These are thought of as primary 
because it is difficult, and perhaps impossible, in some cases to 
appreciate the alimentary errors which are at the bottom of the 
matter. In other cases of so-called primary degeneration typically 
in the nervous system the death of the (neuron) cell, and the con- 
sequent atrophy and degeneration of its processes, may be brought 
about by the agency of very insidious microbic toxins, syphilitic for 
example. This probably is the explanation of many cases of tabes 
dorsalis, and other primary affections of the nervous system not 
directly traceable to inherent weakness. 

To see with the actual or with the clinical eye the process of 
secondary degeneration is usually comparatively easy and simple ; 
for whereas in the primary form the trouble arose from insidious 
qualitative changes in the supply of nutriment and the removal of 
waste, here it is due either to a gross interference with the quanti- 
tative nutritive supply, or to an equally gross mechanical interference 
with the protoplasm of the cells — squeezing or distortion. A few 
illustrations will make the position clearer. The absolute block- 
ing of a large (or microscopical) artery by thrombos is, embolus, or 
ligature, leading to coarse (or fine) gangrene or necrosis of tissue, 
is the most obvious illustration of the former process. It is well 
seen and very common in the brain, spleen, kidney, or lung. It 
occurs, though less commonly, in the intestine, liver, and other 
organs (in surgery it is common enough in limbs, or part of them). 
The secondary degeneration of the processes, long and short, of 
the neuron cells of the nervous system is a less obvious but equally 
c jrtain illustration ; it differs in that the nutritive supply or stimulus 
reaches the process (and indeed probably also gland cells, muscles, 



1 8 DIFFERENTIAL DIAGNOSIS chap. 

etc.) through other channels than obvious vessels, but the degener- 
ative result follows as surely as does general wasting of the body at 
large when the stomach is seriously incapacitated. The actual 
rupture of a vessel may act in both ways ; it is certain that the 
blood supply to the part concerned is stopped, and at the same 
time the blood, escaping from the vessel often at high pressure, 
mechanically tears asunder the cells of the tissue and exposes them 
to every form of distortion and violence. Inflammation, again, in 
its reparative stages, is a potent cause of secondary degeneration 
through the cell strangulation its scar contraction brings about 
(in its acute destructive phases the destruction is wrought by the 
action of poisons and excessive reaction to them), and this not only 
in gross cases of localised trouble, but also in the more chronic and 
diffused forms, as, for example, in cirrhosis of the liver of alcoholic 
origin, in pneumonokoniosis and other forms of cirrhosis of lung. 
The influence of cardiac disease (<?.v.), with its back-pressure stagna- 
tion and increased transudation from the capillaries, acts in a very 
similar manner to the diffuse forms of inflammation — loss of function, 
then death, with a very imperfect or altogether absent power of 
reproduction of cells of highly specialised function, this in turn 
followed by a fine fibrosis to fill the spaces left by the absorption 
of dead cells — these are the processes induced in organs and tissues 
by cardiac failure. 

New Growths. — But one diagnostic difficulty here presents 
itself, and that is of establishing by physical signs the presence of a 
malignant growth. This is frequently great, and sometimes even 
insuperable without surgical aid (will the Rontgen rays ultimately 
assist us here ?) ; but whether this difficulty be overcome or not, 
the pathological processes which a malignant growth starts in the 
body are comparatively simple to understand. Thus a malignant 
growth acts : — 

Mechanically j coarsely 

or > or 

biologically ) insidiously. 

Of the coarse mechanical form of trouble the blockage of a 
hollow tube, either by projection into its lumen or by pressure from 
without, is at once the simplest and most common illustration. Thus 
the intestine, ureter, or bile-duct may be blocked, and gastric dis- 
tension, with vomiting and emaciation, or intestinal obstruction, 
with retention and absorption of fecal products, occur, or retention 
of urine or bile, with a more or less rapidly following toxaemia by 



i DIAGNOSIS IN GENERAL 19 

products that should be discharged from the body. Arteries, capil- 
laries, veins, and lymphatics suffer in precisely the same way, with 
resulting anaemia, or even gangrene, cedema, or effusion, simple or 
chylous, according to the function of the blocked vessel. Solid 
organs, too, may suffer from the same gross pressure, with disturb- 
ance of function and distortion of structure. The brain gives us a 
common illustration of this class, but, owing to the fact that it, with 
its vessels of all kinds, are enclosed in an unyielding box, the 
results are complicated, for they may be due to direct pressure on 
specialised cells, as well as to indirect effects of altered circulation. 

More insidious, but equally real, mechanical (pressure, strangu- 
lation, disturbed circulation) effects are produced by the creeping 
processes of the growth, and explain the symptoms and cause of 
death in many cases, thus in the lung and liver, structure and 
function frequently suffer far out of proportion to the naked-eye 
bulk of the tumour. In the intestine the muscle is paralysed by 
these processes, and so contributes by this paralysis a large share 
to the obstruction. In the brain, too, it is thus that we must 
explain the fatal effects of a small tumour growing into a very im- 
portant area of the organ. This insinuation of the growth into a 
tissue, with violent separation of the elements, frequently sets up a 
diffuse inflammatory reaction in the cells of an organ, and this must 
also be reckoned amongst the insidious mechanical effects. 

The biological or vital morbid processes started by and in 
tumours would seem to depend somewhat upon what we may call 
the physiology of new growths, which may be thus summarised : — 

1. They possess a great power of increase in bulk, or vitality of 
reproduction. 

2. They would seem to possess some form of internal secretion 
or metabolic activity whereby chemical products are poured into 
the blood stream — products which are foreign to the normal 
tissues, and apparently of considerable power for evil in some cases. 

3. They appear to possess but little or even no power of resist- 
ance against irritative, especially microbic, influences. 

(1) has already been considered as starting all the mechanical 
effects, both gross and fine, of tumours. It also explains (microbio- 
logical researches may alter in some ways this view) the phenomena 
of recurrence after apparent extirpation, and metastases due to the 
transference from place to place of cells endowed with this special 
power of reproduction. 

(2) would appear in some measure to explain the anaemia and 
cachexia which frequently, but by no means invariably, accompany 



20 DIFFERENTIAL DIAGNOSIS chap, i 

the existence of a malignant growth. Starvation and the mechanical 
effects mentioned above doubtless play the chief role, but many 
cases occur in which these are not sufficient to explain the great 
cachexia occasionally met with even when the growth does not 
affect an important organ. Thus does a growth insidiously under- 
mine health. 

(3) It is to the feebleness of the powers of resistance (the pro- 
tective reaction to irritation possessed by normal tissues) must be 
largely attributed the ease with which malignant growths become 
the seat of destructive phases of inflammation, with but little cor- 
responding power of allowing or promoting the reparative phases. 
When microbes invade, as they so frequently do, malignant 
neoplasms, they are but seldom killed by the growth, or even 
diminished in vitality, and thus it very frequently, indeed, happens 
that secondary septic processes carry off a patient who begins by 
suffering from carcinoma ; thus in epithelioma of the lips or tongue 
death is very often due to inspiration-pneumonia ; and, indeed, in 
carcinoma of the lung it is as often as not a pneumonia that finishes 
the scene. In carcinoma of the gut, peritonitis is to be feared long 
before perforation can occur, as though the growth encouraged the 
penetration of microbes or their toxins. Such exhibitions may with 
justice be termed the grosser forms of biological active processes 
induced by growths, an empyema or a purulent peritonitis being 
the immediate diagnosis. 

We have thus completed an outline sketch of the primary causes 
and processes of disease. From these, physiological deduction will 
lead us to expect certain morbid phenomena as the result of certain 
untoward influences in our environment. We must now proceed 
to discuss diagnosis by inductive methods, accepting the morbid 
phenomena (the physical signs and symptoms discovered in or com- 
plained of by our patients) as the threads of Penelope to lead us 
out of the maze, or to discover the fountain-head, and thus apply 
therapeutical measures with some idea of what results we hope or 
intend to produce. 



CHAPTER II 

notes on a few of the terms used in medicine and 
medical diagnosis 

Physical Signs v. Symptoms 

Symptoms are those uneasy or abnormal sensations or feelings 
of which the patient complains either spontaneously or as the result 
of verbal inquiry, e.g. pain, cough, shortness of breath on exertion, 
etc. It is customary also to include many other phenomena in the 
term, such as the results obtained by chemical, bacteriological, or 
microscopical research, and even some unusual conditions of the 
nervous system assuredly only found by physical examination, e.g. 
absent knee jerks, etc., but I think it well to have a sharp line of 
distinction where possible. 

Physical signs is a term used to describe those phenomena of 
disease (especially of the chest and abdomen) which only become 
apparent to the observer's senses by means of what is termed a 
physical examination, including, in its completest extent, inspection, 
palpation, percussion, and auscultation in their simple and modified 
{eg. succussion) forms. 

If these definitions are not in every particular absolutely satis- 
factory, they at least form a sound and workable conception for 
clinical purposes. That some such definition as the above is useful, 
my own experience would tend to show, for I have been asked the 
distinction between the two sets of phenomena in a court of law, 
and it is no unfrequent occurrence for a student to glibly enumerate 
a string of the easier and less important physical signs when asked 
for the more perplexing and intricate, and withal more germane, 
symptoms, a reply which may not unfairly be allowed to annoy an 
examiner and create in his mind a bad impression of a candidate's 



22 DIFFERENTIAL DIAGNOSIS chap. 

clinical knowledge. Nevertheless, it must be borne in mind that 
neither in science nor in ordinary usage is there a fundamental dis- 
tinction based on clear conceptions of existing facts. For example, 
pain may certainly be claimed as a symptom, and cardiac bruits as 
physical signs, but what shall we say of the pain-drawn face, or the 
cardiac bruit that is audible and troublesome by its noise to the 
patient ? It follows clearly that where no pressure from counsel or 
examiner is brought to bear, the two terms will be used almost indis- 
criminately. 

Pathology 

No term in medical science is used in such a loose sense, and 
with so many confusing ideas attached to it, as this, and one cannot 
wonder at the student's difficulties in trying to answer a question 
such as, " Give, describe, or state what you know of the pathology 
of such and such a disease." " A chat about the etiology " seems 
at first sight to be a very happy definition, but frequently the term 
is used much more or much less comprehensively. 

It cannot be too strongly insisted upon that there are at least 
three separate and, in some respects, different and distinct ideas 
contained in the word as commonly employed : — 

i. The changes in organs, tissues, and fluids of the body to be 
found by the naked eye and microscope after death = 
morbid anatomy. 

2. The explanation of symptoms (and often, indeed, of physical 

signs also) by reference to the known morbid anatomy ; 
this = morbid physiology or the etiology (from within) of 
symptoms = symptomatology. 

3. The explanation of the morbid anatomy or morbid physi- 

ology by reference to the action or influence of the en- 
vironment on the organism = etiology (from without) of 
disease. 
That all these three meanings may simultaneously be read into 
the word is obvious from its derivation (■7rd6o<; and Aoyos), the theory 
of, or a discourse on, suffering ; but its everyday, and especially its 
examinational, meanings are ill defined. For instance, the path- 
ology of inflammation chiefly concerns itself with the naked eye, 
and especially the microscopical anatomy of the inflamed area and 
the changes going on in its neighbourhood, together with specula- 
tions as to the precise origin of the cells seen. The pathology of 
gout, diabetes, and blood dyscrasias in general, principally requires 



ii TERMS USED IN MEDICAL DIAGNOSIS 23 

a discussion of the primary seat of perverted metabolism, with a 
hypothetical explanation of the morbid physiological phenomena 
which arise in consequence of this perversion, morbid anatomical 
facts receding in the background as results rather than causes ; 
while, again, the pathology of pneumonia or other specific fever 
would be very incomplete without considerable reference to the 
micro-organisms which cause them, and the modes by which these 
parasites enter the body and attack the tissues. 

If no suggestions are given as to the precise form of answer 
required, a clear exposition of the pathology of any disease is best 
given by a brief, concise, but complete as possible, summary of the 
main (anatomical, symptomatic, and etiological) facts observed in 
its history, followed by a statement or discussion of those theories 
which have been propounded as best explaining or linking together 
these facts. 

As an example we may sketch an answer to the question, 
" What is the pathology of cirrhotic kidney ? " 

The most important facts observed in connection with cirrhotic 
kidney are : — 

A. Anatomical. — The almost universal discovery on autopsy 

that hypertrophy of the heart and degeneration of 
arteries have coexisted with the cirrhotic kidneys. 

B. Symptomatic. — The extreme frequency with which patients 

thus afflicted suffer, and even die, from ursemia, cerebral 
haemorrhage, or intercurrent inflammation of some organ. 
The condition of the urine. 

C. Etiological. — That such patients are almost invariably at or 

past middle age, or have been gouty, or suffered from 
plumbism, or suffered from repeated attacks of acute or 
subacute nephritis. 

The theories suggested to account for the anatomy are: (1) 
Johnson's stopcock theory. (2) Gull and Sutton's arterio-capillary 
fibrosis. "Renal inadequacy" (a term associated with the late 
Sir Andrew Clark), especially if of long duration, will largely account 
for the symptoms, while the condition of the kidneys, as revealed 
by the microscope, give a sufficient explanation of this renal 
inadequacy. 

Or, to take a shorter example, the pathology of Addison's 
disease : — 

The only constant anatomical fact is destruction of the supra- 



24 DIFFERENTIAL DIAGNOSIS chap, n 

renal organs, and that almost constantly of a caseous, probably 
tubercular, nature. 

Pigmentation of the skin is not nearly so constant. 

Symptomatic facts are few and summed up in progressive 
debility and frequent gastric crises and a very poor pulse. 

Etiological facts none constant, but tubercle bacilli often found 
in the glands. 

A theory has then to be stated and argued out as to the func- 
tions of the suprarenals, interference with which can produce these 
symptoms ; it must be compatible, too, with the fact that destruction 
of the organs, other than tuberculo-caseous, frequently enough does 
not produce the same symptoms. 



Contagion v. Infection 

These terms are often used to indicate different methods by 
which a disease is communicated from person to person. Unfor- 
tunately (as is so often the case with terms originally possessing one 
specific meaning), habit and common usage, but especially increased 
recognition of facts, have so broken down the limits between the 
meanings, that the words now only remain as puzzles for students. 
Contagion should mean transference by actual contact of person 
with person, while infection should be a more comprehensive term, 
indicating that the disease to which the adjective " infectious " is 
applied can be communicated from one individual to another, and 
should include contact as one method of such communication. The 
essential fact of clinical importance is the communicability of the 
disease; observation and laboratory work must teach us the "how," 
leaving the clinician to use such expressions as "communicated by 
contact," or " by microbes floating in the air and gaining entrance 
to a second individual either by means of milk, water, food, or by 
the breath, etc." Such expressions, if cumbersome, at any rate 
convey a definite meaning ; and until science supplies us with more 
accurate knowledge, " communicable " is quite sufficiently under- 
stood to include all such terms as contagious, infectious, etc. 



CHAPTER III 

MICRO-ORGANISMS AND ZYMOTIC DISEASES 

From communicable diseases to microbes is nowadays hardly a step 
in thought, for the researches of the last quarter of a century have 
taught us that the two are essentially effect and cause. In this 
work, dealing mainly with clinical problems and practical medicine, 
I do not propose to give more than the very briefest outline of 
those fundamental principles of bacteriology which have now be- 
come essential for all medical practitioners. Beyond those principles 
and their correct understanding I do not hold that it is necessary, 
or even desirable, that students or medical men in practice should 
go ; the extraordinary intricate details and scrupulous exactitude 
required for the scientific laboratory working of bacteriology are too 
engrossing for, and demand too much time from, those who do not 
intend to devote their life to purely scientific work of this descrip- 
tion. The healers of the sick must patiently wait for the results of 
laboratory work, recognising and using those which are immediately 
available for practice. These already represent a greater amount of 
accurate and minute knowledge of the causes and processes of 
disease than all the previous centuries have yielded. 

Meanwhile the following numbered paragraphs contain the 
principles of the subject in a form easily assimilable, and only to be 
acquired from monographs by a very tedious process of analysis. 

i. Micro-organisms do exist in countless myriads everywhere in 
nature where the conditions of moisture, temperature, and access of 
air are suitable. 

2. Their genera and species are probably more numerous than 
those of all animals or plants visible to the naked eye. 

3. They are too small to show generic or specific distinctions 



26 DIFFERENTIAL DIAGNOSIS chap. 

in their organs, consequently the classification of them for scientific 
purposes rests on : — 

(a) Gross outward shape — cocci, bacteria, bacilli, spirillum, etc. 

(b) Their methods of aggregation and segregation. 

(c) Motility or the reverse. 

(d) Their chemical and vital reactions to and on their artificial 

environment, e.g. aerobic or anaerobic, whether they liquefy 
gelatine with or without the production of gas, or whether 
they do not liquefy it, what nutrient medium do they 
best flourish in or on ; colour and appearance of the 
growth, etc., etc. 

(e) Their reactions to various staining and decolourising re- 

agents. 
(/) And most importantly, their influence upon their host after 
inoculation into a vein or tissues or serous cavity, etc., 
e.g. whether they produce any symptoms of ill-health or 
not, the character of the symptoms, and the anatomical 
results on autopsy of the animal, etc. In this way 
they have been divided into two broad groups, the 
pathogenic and the non-pathogenic, a distinction which 
frequently breaks down when microbes gain access to a 
part of the body in which they are not usually found, 
e.g. the bacterium coli commune is a natural inhabitant 
of the alimentary canal, but it seems to cause very serious 
mischief when it gets into the tissues generally. 

4. Those now known to produce, and generally accepted as 
producing, disease (the pathogenic group), constitute probably only 
a minute fraction of the whole number of species. 

5. To prove that one particular microbe and no other is the 
cause of a given disease or symptom-complex, the following condi- 
tions must be rigorously fulfilled : — 

(a) It must be constantly found in the blood, tissues, or dis- 

charges of the individuals suffering from the disease in 
question. 

(b) From this source a culture must be prepared in a sterile 

medium, and the particular microbe isolated and grown 
in pure culture for some generations. 

(c) From such absolutely pure culture it must be introduced 

into a fresh healthy individual of the same species as the 
original sufferer. 



in MICRO-ORGANISMS AND ZYMOTIC DISEASES 



27 



(d) This inoculation must reproduce the disease in the second 

individual. 

(e) The special microbe must again be found in the second 

animal in the same situations as before. 

In the strict fulfilment of these laws are contained all the 
difficulties of scientific bacteriology. They can only be appreciated 
by those of experience, and to publish the crude and inaccurate 
results of the dabblers in the science is merely to waste paper, and 
to retard the progress of medicine. 

6. Applied to man and practical medicine there is only one 
microbe which has gone completely through the trial and come out 
triumphant, that is the organism which produces cutaneous erysipelas. 
The reason why no others have been intentionally put to the test is 
self-obvious ; but laboratory accidents (only too frequently), experi- 
ments on animals, and justifiable deduction have so far proved the 
position as to leave no reasonable doubt that a microbe is at the 
bottom of the following well-known diseases : — 



Group I 



Tuberculosis (of every form 

and organ). 
Pneumonia (? one only). 
Anthrax. 
Typhoid. 
Asiatic cholera. 

Diphtheria. j- 

Malaria. 
Leprosy. 

Gonorrhoea (? one only). 
Rabies. 
Tetanus. 
Plague. 



Of which it may be said that the 
type of the disease is fairly con- 
stant, and that one special microbe 
has been identified and universally 
accepted as the essential cause of 
the malady. 



Group II 



Cerebro-spinal meningitis. 

Dysentery. 

Influenza. 

Measles. 

Scarlet fever. 

Small-pox. 

Typhus. 

Varicella. 

Whooping cough. 

Syphilis. 



Of which we may say that the con- 
ditions and circumstances under 
which they occur, together with 
the regularity of their symptoms, 
leave no reasonable doubt about 
each being caused by a definite 
species or genus of microbe, 
though such has not yet been 
satisfactorily isolated so as to be 
universally accepted. 



DIFFERENTIAL DIAGNOSIS 



Group III 



Pyaemia. ) The diseases hitherto enumerated under lists I and 

Septicaemia. ) II have a group of symptoms and clinical courses 

which are so far constant and distinctive (rash, periodicity, anatomical 
products, etc.) as to deserve a specific and constant name, and to lead 
to the belief that one, and one only, species of microbe is the causa 
causans. In these two diseases, on the other hand, the symptoms 
(fairly constant, but with no absolutely pathognomonic feature), the course, 
and careful bacteriological investigation, all tend to raise a conviction 
that more than one, if not indeed several, species of microbes may be 
concerned. To satisfactorily and simply account for the manufacture of 
the words it is necessary to state briefly the clinical classification of 
pathogenic micro-organisms. 

For this purpose, then, we may divide them into three 
classes : — 

(a) Those which, under any circumstances of the patient, are 
able after entry to the body to grow into, attack, and destroy healthy 
tissues, and hence can be, and are, easily carried by the blood- 
stream to distant parts of the body. 

(b) Those which, under no known circumstances of the patient, 
are able thus to attack healthy tissues, but cause symptoms by 
living and growing on dead or dying tissues, and from there dis- 
charging into the blood-stream doses of a chemical poison extremely 
active, indeed, but incapable of multiplication. 

(c) Those which seem to be of an intermediate character, and 
depend for their activity and virulence to a large extent upon the 
conditions of vitality of the tissues upon which they alight, and also 
on their own temporary condition of vigour. 

Pyaemia, then, is a disease produced by a member of class (a), 
and in strictness must include anthrax, and nearly all the other 
specific diseases. 

Septicaemia is a disease produced by a member of class (b). 

Artificial cultivations and experimental inoculations would seem 
to show that between all three groups no line of strict demarca- 
tion can be drawn ; but this does not entirely destroy the clinical 
value of the distinction in cases of disease. For when in a natural 
state the distinction can be moderately well made, and it is prob- 
able that clinical (as opposed to laboratory experimental) diseases 
arise from the invasion of microbes of a natural (to them) healthy 
activity. 

7. Pathogenic microbes would seem to be able to attack tissues 



in MICRO-ORGANISMS AND ZYMOTIC DISEASES 29 

in one or both of two primary ways with a subdivision of the 
second method. 

(a) By a sort of hand-to-hand fight, microbe v. cell = phago- 
cytosis. 

(b) By a weapon in the shape of a secretion = chemiotaxis, 
about which weapon two theories exist : — 

(1) The secretion is itself a poisonous chemical substance = 

a toxin. 

(2) The secretion is of the nature of a ferment, comparable 

to trypsin, say, and = a toxinogen. 

On the other hand the cell defends itself either — 

(1) By bodily eating the microbe. 

(2) By secreting a substance neutralising the toxin, or fer- 

ment, or the products of the ferment ; in either case it 
is called an antitoxin. 

This is the most natural place in which to insert the clinical 
reasons for suspecting that a disease is due to microbial influences. 

(a) The occurrence of an epidemic of the disease in question, 
in which the logic of events seems to prove, or, at least, strongly 
suggest, that on the one hand all the cases arise from a common 
(aerial, aquatic, or telluric) source, from which all gross metallic, 
e.g. lead, copper, arsenic, mercury, or organic, e.g. decomposing 
food, poisons can be and are excluded ; or on the other hand 
that consecutive cases arise from previous ones, the latter a mode 
of spreading often better noticed in the smaller sporadic outbreaks, 
where observation is closer and the methods of "catching" the 
complaint more easily distinguished. 

(b) The existence of localities where endemic diseases flourish, 
where a purely local cause must be at work, but where, again, all 
metallic and ordinary organic chemical poisons can be excluded. 

(c) In both these cases the a priori argument will be enormously 
strengthened by a posteriori reasoning when the common, local, or 
personal factor has been removed, and the disease has ceased to 
attack fresh individuals, and the removed factor has been shown to 
contain no organic or metallic poison. 

(d) The character of the disease itself an active acute onset, 
followed by definite fastigium, with crisis or defervescence, and a 
complete restoration of the patient to health. 

(e) The finding of a definite microbe in the blood, tissues, 



30 DIFFERENTIAL DIAGNOSIS chap. 

fluids, or excretions of the patient. Modern discoveries have 
made this an almost necessary part of routine clinical study, but the 
microbe must be put through the above strict scientific proof before its 
causative role will be accepted. 

Into the extraordinarily fascinating subject of attenuation of 
microbes, causes of immunity, and protective and curative inocu- 
lations I do not propose, further than the observations recorded on 
p. 31, etc., to enter. The work that has been done in this direction 
would fill many libraries were it all published, but it is entirely 
founded on the above principles. 

We will now proceed to consider the differential diagnosis of 
the ordinary zymotic diseases of England. 

For the student to attempt to learn by rote the apparently 
chaotic variations in the incubation periods, symptoms, complica- 
tions, and sequelae of these diseases seems to me a useless, difficult, 
and never-ending task, but to give a working hypothesis as to the 
essential causes of these discrepancies and variations is a compara- 
tively simple matter, bringing rule and order out of confusion. I 
say hypothesis advisedly, because though we have every reason to 
believe that incidents occur in the body in precisely the same 
potential sequence as in the test tube, we have no absolute proof 
that they do so. In the test tube there is no variation from hour 
to hour in the bulk and quality of the cultivation menstruum, 
except such as are brought about by the mixture of bacterial pro- 
ducts ; there are no policemen leucocytes exercising their unceasing 
vigilance in getting rid of foreign substances ; it is doubtful how 
far these cells and the renewal of the menstruum can fundamentally 
change the phenomena, apart from their undoubted power to hinder, 
delay, or prevent them altogether. 

So far, then, as science has allowed us to follow the workings of 
microbes, we are scarcely using the language of metaphor or analogy 
when we speak of the invasion of the body by specific germs 
in precisely the same terms as we use when describing the invasion 
of a geographical country by a hostile nation ; the differences 
between the engaging forces are almost nothing but those of size 
and the nature of the weapons used. 

The first event, then, is an attempted landing of the invading 
forces. To say that the expedition may be wrecked by storms on 
sea or land is nothing more than to say that multitudes of malignant 
and pathogenic microbes enter the apertures of the body or alight 
on the skin, but are immediately swept away by the forces of respira- 
tion (sneezing, coughing, etc.), by food and drink, by smoking, by 



MICRO-ORGANISMS AND ZYMOTIC DISEASES 31 



accidental rubbing of clothes, by washing, etc. ; that, in fact, they 
never get a foothold in the tissues or blood. 



Date of infection. 



Incubation period. 



Reason why in an 
epidemic all ex- 
posed do not 
sicken ; meaning 
of immunity ; ab- 
ortive cases also. 



Malaise of incuba- 
tion period. 

Onset sudden or 
gradual. 



Ingravescence of dis- 
ease and fasti- 
gium. 

Defervescence, or 
crisis, or death. 

Convalescence and 
death from ex- 
haustion in it. 



A successful landing is the moment of infection, 
and from now onwards we have the varying 
incidents of a campaign. 

The invaders have to strengthen their position, 
increase their numbers (for our story it is im- 
material that they do this with inconceivable 
rapidity by reproduction), and provide food ; the 
time thus occupied represents the incubation 
period. 

Even now, or at a somewhat later stage, when 
the march through the country has begun 
(abortive cases), a complete miscarriage of 
the whole expedition may occur through (a) a 
want of suitable food in the district, or (0) the 
energy of the local inhabitants and first line 
of home defences, who may annihilate the in- 
vaders as soon as they emerge from their local 
camp. It is possible in either or both of these 
ways to explain immunity, natural or acquired, 
permanent or temporary only. 

The slight excitement caused by the rumours of 
an invasion represent the malaise and slight 
symptoms of the incubation period. 

The relative strengths of the contending parties 
explain the nature of the onset. In one set 
the invaders are so powerful, or have become 
so numerous, that their attack and onward 
march cause the utmost consternation through- 
out the land ; in the other they are so insigni- 
ficant in strength or numbers that only a slight 
disturbance is caused at first, though later 
their power may be enormously increased by 
reinforcements, etc. 

As the invaders march through the country the 
war rages with increasing violence, until either, 
in repeated conflicts, or in one great pitched 
battle, the invaders are destroyed, or per contra, 
the defenders are completely defeated. 

When the invaders have been thoroughly routed 
comes the time for rebuilding cities, towns, 
and villages, and for recuperation of the in- 
habitants, and it may happen that the whole 



32 



DIFFERENTIAL DIAGNOSIS 



Persistent debility, 
or even stronger 
than ever. 

Complications and 
sequelae. 

(i) Specific to the 
disease, e.g. otor- 
rhoea. 

(2) A second specific 
disease succeed- 
ing the first. 



(3) Non - specific 
complications, e.g. 
abscesses from 
pyogenes, coli 
commune, etc. 



nation is so exhausted that this is impossible, 

and life ceases in the country. 
Rebuilding and renovation may remain for ever 

incomplete, or may be such as to make the 

country stronger than before. 
In such a war of invasion there may be found 

three well-marked classes of events : — 

(1) The attacks on the principal cities by the 
original invaders. 

(2) A separate descent upon the country of a 
different invading force, which, eating different 
food, or fighting with different weapons, may 
go through all the vicissitudes of the first 
force. 

(3) Turbulence and riot on the part of a mal- 
content native or alien population which had 
previously, under pressure from local authority, 
lived more or less quiet, and even useful, lives. 



Dropping now the possible suspicion of using metaphorical 
language, we know for a certainty we have the following variables 
in every equation of infectious disease : — 

1. The inherent constitution of the individual's tissues, cells 
and body fluids, including the presence or absence of certain 
materials for the growth of microbes, the power of manufacturing 
antitoxin, or of eating up these microbes. 

2. The quasi-accidental temporary powers of the same at the 
time of infection. 

3 and 4. Similar powers on the part of the invading microbes. 

5. The actual number of the latter gaining admission (antago- 
nism between different microbes landing at the same time). 

Scientific laboratory work has proved beyond all doubt that 
each of these is of the utmost degree of importance, but it has not 
given us even an inkling as to the laws which govern the variations 
on the part of the body forces, and is only on the threshold of in- 
vestigations into those regulating the microbes ; the strongest men 
often enough fall victims to epidemics while the weaklings escape, 
some in contact with the patients are smothered with microbes and 
escape, while for others or even the same persons at another time, 
a single contact is sufficient to produce a most virulent attack. 

Although these unknown variables and their unknown laws make 



in MICRO-ORGANISMS AND ZYMOTIC DISEASES 33 

any tables of comparatively little scientific value, the following 
may be found of some practical utility in clinical work as well as for 
examination purposes. 

Table of Incubation Periods 



Anthrax . 






2 or 3 days. 


Cholera . 






up to 1 5 „ 


Diphtheria 




Have been known to 


2 to 4 „ 


Influenza. 




develop within 24 hours 


3 or 4 „ 


Pneumonia 




of infection, though the 




Relapsing fever 




annexed periods in 


4 to 10 ,, 


Scarlet fever 




days are very much 


2 to 5 „ 


Septicaemia 




commoner. 




Tetanus . 






Up tO 2 I „ 


Yellow fever 


j 




^ up to 18 „ 


The following, arranged roughly in order of duration, are : — 


Gonorrhoea 


2 to 3 days. Pertussis . . 6 to 1 2 days. 


Typhus . 


2 to 12 „ Measles. . . 8 to 12 „ 


Glanders 


3 to 18 „ Malta fever . . about 10 „ 


Typhoid 


4 to 20 „ Rotheln . . . 10 to 21 ,, 


Variola . 


. 1 1 or 1 2 days (curiously constant). 


Varicella . 




. 10 to 14 „ 


Erysipelas 




. 10 to 14 „ 


Mumps . 




. 12 to 21 „ 


Syphilis . 




. 18 to 28 „ 


Rabies 




. 40 days and upwards 


Tubercle . 




. Unknown, probably 


some weeks. 



Our previous considerations have led us a priori to expect what 
we actually find, viz. that the variations are much too great and 
too irregular to serve any diagnostic purpose ; but they explain why 
three weeks has been adopted as the period of segregation of 
individuals who have been exposed to infection, where such 
segregation is possible, as in schools and public institutions. 

When the incubation period is at an end, and the actual onset 
of the disease begins, diagnosis rapidly narrows itself down. Many 
of those enumerated above show characteristic features, apart from 
pyrexia, almost at once, thus : — 

Anthrax . . . Ring of vesicles with central black slough. 

Cholera . . . Characteristic diarrhoea, except in fulminat- 

ing cases. 
D 



34 DIFFERENTIAL DIAGNOSIS 



Diphtheria . 




Membrane on infected spot. 


Pneumonia . 




Cough and disturbance of respiratory rhythm 
vide p. 35. 


Wound-Septicaemia 


Wound inflamed and discharging. 


Gonorrhoea 




Urethral trouble. 


Syphilis and 


venerea] 




poisons 




A chancre of some description. 


Glanders 




Particularly acrid nasal discharge. 


Erysipelas 




Sharply defined red blush surrounding a 
wound. 


Tetanus 




Stiffness of jaws, or abdominal muscles. 


Mumps 




The swelling of both parotids. 



The bulk of the remainder is constituted by the common so- 
called zymotic diseases or exanthems of our country. In them the 
presence of an epidemic gives the primary and the strongest clue to 
the diagnosis. I might go so far as to say that in many aberrant 
and abortive cases this forms the only guide, for without it many 
cases of sore throat, or of rashes in a scarlet fever epidemic, of 
nasal catarrh in an outbreak of measles or influenza, would go 
unrecognised. Next to epidemicity, the manner of onset in fairly 
typical cases gives the best clue to differential diagnosis. Thus 
they are all accompanied with pyrexia, which in — 



Influenza 
Relapsing fever 
Scarlet fever 
Typhus 
Variola 

Measles 
Pertussis 
Rotheln 
Typhoid 



Almost invariably comes on very rapidly, 
reaching its probable maximum within 
twenty-four hours. 



Comes on much less rapidly, taking two 
or three days or even longer (especially in 
typhoid) to reach its height. 



After the onset a period elapses, nearly constant for each 
zymotic, before the further diagnostic point of the characteristic rash 
is available. We may utilise this period to draw attention to those 
symptoms which, if not actually the result of a temperature above the 
normal (a point made doubtful by manyconsiderations), are at any rate 
the twin results with pyrexia of the toxaemias of disease. They are 
very important, as, when they are present, they suggest the continual 
use of the clinical thermometer ; they also give the student a 
rational and firm basis for a written description of the symptoms of any 



MICRO-ORGANISMS AND ZYMOTIC DISEASES 



35 



zymotic, of which indeed, with the rash, they form the bulk, stress 
being only laid on special points. 

Following the plan laid down on p. 2, we have : — 

The Symptoms of Pyrexia 



Tongue. 

Appetite. 

Thirst. 
Bowels. 

Respiratory and 
vascular 
symptoms. 



Urinary system. 



Skin. 



Alimentary System 

Usually a tendency to get dry and dirty, in 
typhoid and in scarlet fever often typical. 

Much diminished, probably digestion is nearly in 
abeyance. 

Almost constantly increased. 

Constipation the rule, in measles and typhoid 
diarrhoea not uncommon. 

The respiration and pulse are quickened, and in 
simple case in their ordinary ratio of 1 to 
2-|-. It is a sufficiently accurate and good 
clinical rule to expect an increase of about 1 o 
beats per minute in the pulse rate for each 
degree F. that the temperature is over the 
normal. The principal exceptions are scarlet 
fever, in which the pulse rate is often acceler- 
ated out of all proportion, and influenza, in 
which there is very little acceleration. If the 
ratio of i\ to 1 is markedly altered, pulmonary 
or cardiac (endo- myo- or peri-cardial) compli- 
cations must be strongly suspected and care- 
fully looked for. 

The urine is usually diminished in quantity, 
increased in colour and specific gravity ; urates 
are very frequently deposited in excess on 
cooling. There seems to be no doubt that the 
toxins of all diseases are irritating to the 
kidney (by which channel they are largely 
excreted), hence the presence of a trace of 
albumen is very common ; it has little signifi- 
cance either as a signal of future kidney dis- 
ease, or as a diagnostic point, except in scarlet 
fever, where obstinate nephritis is an only too 
frequent sequela, and in diphtheria, when 
albuminuria helps to decide the nature of an 
otherwise doubtful sore throat. 

Is often hot and dry, or may be moist and 
covered with sudamina. 



36 DIFFERENTIAL DIAGNOSIS chap. 

Nervous system. Headache, especially at back of eyes, a feeling 

of languor and debility with aching sensations 
in the limbs and back more or less severe, 
and the consequent restlessness, are all that 
can be ascribed to ordinary pyrexia ; should 
the temperature be over 105° delirium or 
coma may supervene, but these, with subsultus 
tendinum, floccitatio, etc., belong much more 
to poisoned than to heated blood, and may be 
seen with a subnormal temperature. It is 
worth while to note that small-pox, even 
in comparatively mild cases, is associated 
with a back - ache of quite disproportionate 
severity. 

The characteristic rash of each disease now begins to appear, 
almost constantly as in the table below. With its appearance, 
though probably long before, the diagnosis will be complete. 

Such are the usual features of the rashes of our zymotics, and 
they will, if anything like typical, be found sufficient to finally clinch 
a diagnosis which even for the most experienced may have remained 
doubtful previous to the appearance of the rash. 

Desquamation. — Inasmuch as desquamation is usually considered 
very strong if not conclusive evidence in favour of a past infectious 
disease, it may not be out of place to state definitely once for all 
that it may be seen of almost any degree and character in patients 
who have been in bed for any disease. It is extremely copious in 
the course of some skin affections (dermatites), also after excessive 
doses of thyroid gland, and after prolonged (some days) bathing, as 
in typhoid ; but I have also seen it after pneumonia, in the course 
of kidney disease, as well as in patients affected with chronic spinal 
cord mischief. 

We have now concluded the symptomatological diagnosis of our 
infectious diseases ; it simply remains to tabulate a few of the 
most salient features of contrast of the individual affections which 
are likely to be confounded, or which are of special interest to 
students. 



[Table 



MICRO-ORGANISMS AND ZYMOTIC DISEASES 37 



Table referred to on page 36 



Disease. 


Date of Rash after 
Onset. 


Locality. 


Characters. 


Varicella 


Within 24 hours 


Anywhere, fre- 


Clear vesicles, not 






quently several 


umbilicated, but 






crops of them. 


they often leave 
scars. 


Scarlet 


Within 48 hours 


Chest first, rapidly 


Bright, boiled-lobster 


fever 




spreads to trunk, 


colour, disappears 






face, and limbs. 


on pressure (except 
in malignant cases), 
followed by large 
flaky desquama- 
tion, which con- 
tinues longest on 
hands and feet. 


Rotheln. 1 


About 3rd day 


Trunk 


Mottled like measles, 
or red like scarlet 
fever, followed by 
small branny des- 
quamation. 

At first felt rather 


Variola 


3rd day 


Forehead first, but 






soon nearly uni- 


than seen as a soft, 






versal ; only one 


velvety feeling of 






crop, v. varicella 


skin with nodules 
under it ; soon um- 
bilicated vesicles, 
becoming pustules 
in 4 or 5 days, and 
almost invariably 
leaving scars. 


Measles 


4th day 


Forehead first, 


Mottled, patchy, does 






and limbs, soon 


not absolutely dis- 






spreads to trunk 


appear on pressure. 
Desquamation is 
small and branny. 


Typhus 


5th day 


Wrists very early, 


Mottled and haemor- 






soon universal. 


rhagic spots, not dis- 






One crop only. 


appearing on pres- 
sure, conspicuous. 


Typhoid 


7th or 8th day 


Abdomen and back, 


Small red, slightly 






successive crops 


elevated spots, dis- 
appearing on pres- 
sure, and usually 
want looking for. 



1 There is some dispute as to the existence of this disease ; its clinical features, as 
allowed by the believers in it, are exactly intermediate between scarlet fever and 



38 DIFFERENTIAL DIAGNOSIS 



VARICELLA v. VARIOLA 

Fever and constitu- Scarcely marked, and Usually very severe, 
tional symptoms. even if pyrexia and especially the 

severe, still not back-ache, 

much constitutional 
disturbance. 
Date of rash. First day. Anything in first two 

days will be prelimi- 
nary atypical and 
probably hasmor- 
rhagic ; typical rash 
on third day. 
Rash itself. Often successive crops, Always one crop only, 

non - umbilicated, Umbilicated and 

hemispherical; often confluent, 

practically never 

confluent ; contents Contents always puru- 
rarely more than lent ; forehead al- 

milky ; appear any- most always the 

where. first. 

It is but very rarely that any serious difficulty arises in the 
differential diagnosis of these two diseases, only an extraordinarily 
severe case of varicella could be mistaken for a mild attack of 
modified variola and vice versa. It is well to emphasise the fact 
(usually unnoticed or denied) that varicella does frequently leave 
pitted scars which may easily be mistaken individually for those left 
by smallpox, their greater number after the latter will be the best 
guide. 

VARIOLA v. SYPHILIS 

A far more difficult problem may occasionally arise to decide 
between the rash of variola and a varioliform syphilide. In both, 
the fever and constitutional symptoms may be very severe, and the 
actual spots may be identical in appearance, umbilicated and puru- 
lent. The most reliable point will be the situation of the rash, 
which in syphilis is nearly sure to be confined to the forehead, where 
it may be very copious ; it is almost certain to be much more widely 
spread in variola. If doubt remains, a history of a chancre must be 
sought, and may clear up the diagnosis. 



in MICRO-ORGANISMS AND ZYMOTIC DISEASES 39 



DIPHTHERIA v. 



'HOSPITAL," OR 
SORE THROAT 



ULCERATED 1 



The following points are usually made in separating these 
troubles : — 



Diphtheria. 

Always derived from a previous 
case. 



Temperature not high as a rule, 

io2° maximum. 
False membrane includes necrosed 

epithelium, if removed leaves a 

bleeding raw surface. 
Albuminuria. 
Knee jerks often lost, and neuritis 

as sequela. 
Klebs-Loeffler bacillus found. 



Ulcerated Sore Throat. 

May arise de novo (at least with- 
out known exposure to previous 
throat case), from smell of 
drains, septic wounds, etc. 

Temperature higher, on an average 
101° to 105 . 

False membrane only an exudate, 
if removed does not leave a 
bleeding surface. 

No albumen in urine. 

No loss of knee jerk or neuritic 
sequela. 

Other microbes but not the Klebs- 
Loeffler. 



Notwithstanding the discovery of the Klebs-Loeffler bacillus, 
which must be by all admitted as the only cause of one specific 
form of disease called by the name of diphtheria, I am strongly 
convinced, as the result of personal experience, that there are 
several kinds of microbes which can give rise to forms of ulcerated 
sore throat, which by every clinical test are indistinguishable from 
the diphtheria produced by the Klebs-Loeffler bacillus ; there may 
be sloughing and bleeding on removal of the slough, there may be 
albuminuria, and possibly disturbance of function of peripheral 
nerves — in fact, everything. 

This statement may be accepted without its being held that I 
am preaching a dangerous doctrine, for I hold that the same care 
should be given to every case of ulcerated throat, and that the 
same isolation, especially as regards kissing and breathing the 
breath of the patient, should be practised, whatever the microbe 
may be, for all such cases are undoubtedly infectious. Nor do I dis- 
approve of the use of antitoxin. I hold very strongly that if the 
throat be due to the Klebs-Loeffler bacillus, the injections will 
cure, when the case without them would be hopeless ; and if the 



40 



DIFFERENTIAL DIAGNOSIS 



throat be due to other microbes, the injections will certainly do no 
harm. 

It may be that the acceptance of my view tends to vitiate the 
statistics of diphtheria, and hence those of antitoxin cures. This 
I cannot help, for I believe I am stating truth, and that even the 
most experienced will admit it. The confusion — if confusion 
there be — is due to the fact that we do not yet know all the 
powers for evil of all microbes, nor the laws which govern their 
growth on human tissues, and the powers of resistance of these 
same tissues. 

We have already noted that rotheln as a distinct disease is 
not recognised by some observers. Accepting its existence, how- 
ever, the following table, constructed from Dr. Roberts' Medicine, 
shows the principal characters of the three diseases — rotheln, 
measles, and scarlet fever — their likenesses and contrasts : — 



MEASLES 



ROTHELN 



SCARLET FEVER 



Incubation 

Eight to twelve days, Ten to twenty days, Two to five days, 
never a few hours never a few hours often within twenty- 
only, only. four hours. 



Fairly sudden, with 
rapid increment. 



Onset 

Sudden, but gets no Very sudden, acme in 
worse. twelve hours or so. 



Symptoms of Onset 

Catarrh of nose and Sore throat, but not Throat symptoms very 
eyes. so bad as scarlet prominent, 

fever. 



About I02 c 



Temperature 
io2° or lower. 



102° or higher. 



Rash 

Appears about fourth Appears second day, Appears in twenty-four 

day, distinctly to be papules brighter hours, not raised nor 

felt,mottled patches, than in measles but to be felt, large 



in MICRO-ORGANISMS AND ZYMOTIC DISEASES 41 



does not completely 
disappear on pres- 
sure, symptoms soon 
lessen when rash 
appears, rash lasts 
three or four days. 



Proportional to fever. 



patchy, may coal- 
esce and be bright 
like scarlet fever. 
Symptoms nearly 
gone when rash ap- 
pears, rash lasts al- 
ways four or five 
days, and may be 
eight or ten, longer 
than either of the 
other two. 

Pulse 
Proportional to fever. 



areas, uniformly 
bright red ; disap- 
pears entirely on 
pressure; symptoms 
worse if anything 
when rash is at its 
height ; rash lasts 
four or five days. 



Frequent, out of pro- 
portion to fever. 



Varieties (only to be noted in Epidemics) 

Sine eruptione, sine No marked varieties, Sine eruptione, angi- 
catarrho, malignant but may occasion- nosa (throat speci- 

(haemorrhagic). ally be rather severe. ally bad), maligna 

(hemorrhagic). 



Sequelae and Complications 



Eyes, nose, and ears, 
but especially cat- 
arrh of air passages, 
also catarrh of in- 
testinal tract. Can- 
crum oris. 



None usually ; very 
rarely nephritis. 



Nephritis and dropsy, 
rheumatism, ear dis- 
ease, endocarditis, 
cellulitis of neck, 
cancrum oris, ab- 
scesses. 



Without the rash and without the presence of an epidemic to 
guide one, there are no features that will enable a diagnosis to be 
made between some cases of bad sore throat and the throat which 
may accompany either scarlet fever or (occasionally) measles. 

Quite recently there have been described small whitish spots 
on the mucous membrane of the mouth and palate, which are said 
to be a pathognomonic indication of incipient measles. 



TYPHOID v. TYPHUS 



Typhus. 
I. Only seen in crowded poor 
communities ; almost absolute 
contact required for infection. 



Typhoid. 
Epidemics common in sparsely 
populated districts, conveyed by 
milk or water to a distance. 



42 



DIFFERENTIAL DIAGNOSIS 



Typhus. 

2. Incubation, two to twelve days. 

3. Onset very sudden. 

4. Symptoms markedly nervous 
and cerebral. 

5. Rash prominent to eye, as 
much on limbs as body, usually 
hemorrhagic, appears earlier 
than in typhoid, five or six 
days. 

6. Constipation the rule. 

7. Crisis almost invariable ending. 

8. Complications septic in charac- 
ter anywhere in the whole body. 



9. No characteristic lesions after 
death. 



Typhoid. 

2. Very indefinite, may be a fort- 
night or more. 

3. Onset usually insidious, but may 
be rather sudden. 

4. Symptoms markedly gastroin- 
testinal, though headache often 
severe. 

5. Rash usually requires to be 
looked for ; almost confined to 
trunk ; rarely more than ery- 
thematous spots, entirely dis- 
appearing on pressure, rarely 
present in first week. 

6. Diarrhoea the rule, at any rate 
in second week. 

7. Lysis almost invariable ending. 

8. Chief complications abdominal, 
— perforation, peritonitis, or 
haemorrhage, but periosteal ab- 
scesses not very uncommon. 

9. Characteristic lesions of intes- 
tines. 



Considering the absolute contrasts that these two diseases 
offer, it would seem impossible that they should have been so long 
confounded ; but we must remember that in those days typhus was 
very much more common than now, and therefore there were 
probably many cases aberrant from the type. If we remember, 
too, that what is now known as the " typhoid state " (dry, brown 
tongue, delirium, subsultus tendinum, and collapse) is the charac- 
teristic condition of any severe blood-poisoning of any nature, we 
may cease to wonder at the confusion. 

The separation of the two is now of almost purely academic 
examinational (and historical) interest, for typhus is so rare that 
scarcely 1 per cent of medical men ever see a case. 

The above table is quite sufficient should the differential 
diagnosis be required. 

WeidaPs test (the influence of the serum of a suspected person 
upon cultivations of typhoid bacilli) has recently been discovered. 
Its reliability would up to date seem to be of the very highest 
degree, in fact almost absolute if done by a skilled bacteriologist. 



in MICRO-ORGANISMS AND ZYMOTIC DISEASES 43 

CHOLERA ASIATICA v. CHOLERA NOSTRAS (Severe 
Diarrhoea or Ptomaine Poisoning) 

In England, luckily, we are not often called upon to deal with 
an epidemic of true Asiatic cholera ; but, frequently enough, it is 
imported into our seaports, and occurs sporadically from this 
origin, so that the diagnosis is of some importance. 

The essential etiological pathology of all such intestinal fluxes 
is the same. An irritant reaches the intestinal canal and causes a 
severe diarrhoea, to which, in the main, and not to the specific 
nature of the irritant, the symptoms are due. The diagnosis must 
then eventually rest upon the scientific discovery or proved absence 
of the comma bacillus of cholera, but the following clinical points 
are worth bearing in mind : — 

1. If the outbreak or case be due to some ordinary irritant 
(chemical or living) in the food there will usually be an obvious 
history of such being the case, e.g. a public dinner, or all the mem- 
bers of a family being simultaneously attacked after a meal. 

2. Children are almost the exclusive sufferers from our summer 
diarrhoea. If adults are also attacked, then paragraph (1) is 
nearly sure to be true. 

3. In food-poisoning cases all the patients will be attacked so 
nearly simultaneously or under such circumstances as to exclude 
the possibility of infection from patient to patient. 

4. Cholera nostras occurs with us almost exclusively in very 
hot summer weather, or in the autumn, when there is much spoiled 
fruit about. 

5. Rice water stools are said to be very typical of true cholera, 
They are seldom passed by patients with ptomaine poisoning. 

6. In a fatal case, with none of the above guiding indications, 
bacteriology must be called upon for the diagnosis. 

ERYTHEMA SIMPLEX v. OTHER RASHES 

To separate simple erythema from the erythematous rashes of 
more serious disease is a problem rather frequently arising in 
children. A new blanket, or underclothing of wool, a little dys- 
pepsia, will frequently produce a rash closely resembling that of 
scarlet fever or erysipelas. In all cases of the slightest doubt an 
appeal must be at once made to the clinical thermometer, and again 
in twelve hours or so. Two or three observations on the tempera- 



44 DIFFERENTIAL DIAGNOSIS chap. 

ture will clear up most cases. There is seldom pyrexia, at any rate 
of more than a few hours' duration, with the simpler troubles, and 
still less frequently an apyrexial condition when infectious disease is 
the cause of the rash. Besides the temperature the following 
points will be of assistance : — 

Erythema. Erysipelas, etc. 

Margin of rash gradually fades into Outline of blush very distinct, 

healthy colour. Locality erratic, Locality usually recognisable as 

no discoverable wound. that of a specific fever, or round 

a wound. 

No constitutional disturbance, Usually considerable disturbance 

headache, vomiting, or chilliness. of bodily health. 

Probable history of some contact Probable suspicion of infection, 
with irritating clothing material 
or known slight trouble. 

Little tendency to spread after once Usually spreads distinctly under 

it is out and discovered. observation, while symptoms re- 
main or get worse. 



INFLUENZA 

Of late years we have had a repeatedly recurring recrudescence 
of this pest, and many opportunities for establishing its differential 
diagnosis. In the several epidemics it has almost seemed as 
though we had as many separate diseases to deal with — now an 
outbreak of contagious meningitis, now a pulmonary epidemic, and 
now one of gastro-intestinal catarrh or worse. In some a severe 
catarrh of the nose and eyes with a mottled rash has aroused suspi- 
cion of measles, while in others a severe tonsillitis and a bright red 
rash have made a diagnosis of scarlet fever seem almost justified. 

The view which seems to me to best explain these vagaries is to 
assume that the microbe of influenza (it has not yet been isolated 
to the satisfaction and acceptance of everybody, though its existence 
is universally believed in) has but little specificity of its own. If it 
has a particular affinity it is for the nervous system, which it attacks 
with undue violence, causing disproportionate headache and pains, 
and followed by a debility out of all proportion to its pyrexia. 
Should the victim of its attack possess, however, a distinct locus 
minoris resistentiae it will attack that locus, and cause what is 
apparently a simple non-specific inflammatory attack, a pneumonia, 
a nephritis, a tonsillitis, a diarrhoea, etc. 



in MICRO-ORGANISMS AND ZYMOTIC DISEASES 45 

As regards its actual diagnosis, my own experience would lead 
me to say that in cases uncomplicated by any actual inflammatory 
disease of an organ its main characteristics are : — 

1. The absolute suddenness (even to the minute) of the onset 
of malaise and chilliness. 

2. The presence of pyrexia, above 99.5 say, separates it from 
an ordinary cold in the head, especially in conjunction with — 

3. The great intensity of the aching in the limbs and eyes. 

4. During the first twenty-four to forty-eight hours the diag- 
nosis, at least in children, must remain in doubt if any other 
epidemic is about. 

5. At the end of this period, when we are expecting a rash or 
some other specific symptom, the temperature falls, and the patient 
is convalescent, unless some definite complication has occurred. 

6. If such a local affection arise, the fact that it is due to in- 
fluenza can only be determined by the prodromal symptoms which 
are absent in the simple cases. 

In those cases where a rash and coryza or tonsillitis occur a 
certain and unquestionable diagnosis is at first impossible, unless 
there be a definite epidemic of influenza in the air, but we may 
remember : — 

(a) The rash is more evanescent in influenza than in scarlet 
fever or measles. 

(3) The whole febrile period without complications is also much 
shorter. 

(c) Scarlet fever and measles but seldom occur more than once 
in a lifetime, and therefore a previous history of either is pro tanto 
a point in favour of influenza. 

(d) Just the reverse holds of influenza, and a previous attack 
makes the present one more probably of that nature. 

(e) In adults first attacks of scarlet fever and measles are com- 
parative rarities, while influenza may have its first incidence at any age. 



VENEREAL INFECTIOUS DISEASES 

These include gonorrhoea, syphilis, and septic inoculations. 

The diagnosis of gonorrhoea, with its special power of producing 
a suppurative discharge from mucous membranes, need not delay 
us. It is the truthfulness of the history more than the nature of 
the urethritis that requires consideration. 

To differentiate a simply septic venereal sore from a true 
syphilitic chancre is much more difficult, and the fact that the 



4 6 



DIFFERENTIAL DIAGNOSIS 



syphilitic and septic microbes are, with extraordinary frequency, 
inoculated together and grow side by side renders it often impos- 
sible to tell whether a given sore will ultimately prove syphilitic or 
not. Remembering, then, that many sores are both, the following 
points must be taken only as guides, not as infallible supports : — 



Septic. 
Incubation only a day or two. 



Syphilitic. 

Some three weeks. A sore (the date 
of inoculation for which can be 
sworn to) cannot be purely syphi- 
litic if it appears within a week, 
but it may be both. 

Pure syphilis does not suppurate, 
and probably not ulcerate ; but 
if a sore does ulcerate and 
become phagedenic, it is curious 
that it almost always contains 
also the syphilitic virus. 

Most usually single, and cannot be 
inoculated on to a distant part 
of the body. 

Induration is sharply defined like a 
wad let into the skin. Is some- 
thing special to syphilis, not 
simple inflammatory. 

Bubos are hard and isolated, and 
if due purely to syphilis have no 
tendency to suppuration. 

Rash and sore throat coming on 
some weeks later are the only 
real pathognomonic features of 
true syphilis. 

One cannot too strongly insist on the fact that a very large 
majority of venereal sores have the syphilitic virus in them, though 
its presence is for a long time obscured by the more active and 
rapidly-developing septic microbe, the work of which is soon pro- 
minent enough. The positive features of syphilis may later become 
most distinct, but a negative is proverbially difficult to prove, and 
nothing but six months from the date of inoculation will prove it 
satisfactorily. The question whether this is too heavy a price to 
pay for certainty belongs to the region of treatment, and cannot be 
discussed here. 



Suppuration ana ulceration fairly 
free. 



Frequently multiple, and can be 
inoculated on to a separate part 
of the body intentionally or acci- 
dentally. 

Induration, if present, fades off 
gradually, and is only inflam- 
matory oedema. 

Bubos often form, enlarge, soften, 
and abscess forms. 

No rash, sore throat, or other con- 
stitutional disturbance at a later 
period. 



CHAPTER IV 

DISEASES OF THORACIC ORGANS 

Section I. — The Lungs and Accessories 

The principal symptoms arising from disease within the thorax 
are : — 

(i) Pyrexia. 

(2) Alterations in respiratory movements and rhythm. 

(3) Alterations in cardiac sounds, position, and rhythm (vide 

Section II). 

(4) Pain, and — 

(5) Various other pressure effects. 

The physical signs consist of alterations in the normal or 
average condition noticed on — 

(1) Inspection. 

(2) Palpation. 

(3) Percussion. 

(4) Auscultation. 

I propose first to analyse some of these phenomena from the 
point of view of diagnosis, and then to offer a few remarks on the 
individual diseases producing them. 

PYREXIA 

This, qua thoracic disease, is only likely to be present as the 
result of inflammation of some thoracic organ, or produced by 
nervous reflex from irritation of the vagus, with or without inter- 
ference with respiration or circulation. 

Of the latter form there is but little in an elementary book to 



48 DIFFERENTIAL DIAGNOSIS chap. 

say. It would certainly seem that hyperpyrexia might sometimes 
arise from this source, for it is seen occasionally in cases of peri- 
carditis and pleurisy, and when rheumatic hyperpyrexia is accom- 
panied by visible organic disease, this is almost constantly a 
pericarditis, so that arguments are not wanting to establish the 
position of a reflex hyperpyrexia through vagus irritation, though 
other factors, e.g. the rheumatic poison, may have a good deal to do 
with the temperature variations. 

In cases of organic disease of the intrathoracic organs, on the 
other hand, the thermometer affords many useful points in differ- 
ential diagnosis. In cases, for instance, where the physical signs 
tell us that bronchitis is present, it is a common rule of practice to 
consider that a temperature of ioi° or over indicates the extension 
of the inflammatory process to some of the alveoli, so that broncho- 
pneumonia is present, even though there be no tubular breathing, 
etc., suggestive of consolidation of lung, within the range of the ear. 
Again, we may suspect that an undoubtedly catarrhal area has been 
invaded by tubercle, or we may think of tubercle when a persistent 
cough exists without physical signs of a catarrh ; here a nocturnal 
elevation of temperature with a normal reading in the day is a very 
strong piece of evidence in favour of the more serious condition, 
though it must be admitted that tubercle is sometimes apyrexial, 
and simple catarrh may be febrile even after its acute stage has 
passed. Lastly, in pleurisy with effusion, a nocturnal elevation of 
temperature, especially if associated with sweating, strongly suggests 
that the effusion is purulent, or, if proved clear, that it is due to 
concealed tubercle. The non-subsidence of a pyrexia after apparent 
removal of the cause, e.g. tapping, must be carefully watched to 
ascertain the meaning of the hitch in the proceedings ; and similarly 
when a pyrexia, whose cause is known and whose course is usually 
constant, as in the common zymotics, does not follow the average 
rule, pulmonary complications must be suspected and carefully 
looked for. 

It is important to remember that when breathing power is very 
seriously interfered with, as in some cases of pneumonia or broncho- 
pneumonia, or in an ordinary case of bronchitis becoming capillary, 
the temperature may sink and become normal, or more probably 
subnormal, while the disease is making rapid strides to a fatal issue, 
so that a subnormal temperature in such cases is even more to be 
feared than pyrexia of moderate, or even severe degree, say up to 
103.5 or io 4- The same may be said in severe cardiac failure 
from any cause, though increased temperature is here less likely as 



iv DISEASES OF THORACIC ORGANS 49 

an initial phenomenon except in recent endocarditis, of which, 
indeed, pyrexia and a bruit are the chief indications. 

In all cases of old or chronic lung and heart mischief, the 
thermometer is an important aid in determining whether the 
physical signs are produced by old changes in the tissues or by 
active processes still going on. If the former, there will most prob- 
ably be no fever ; if the latter, pyrexia may be present ; at least if 
pyrexia is present, then the changes are probably active. 



Alterations in Respiratory Rhythm 
(a) Cough 

Cough, as we know, is a peculiar modification of respiration 
which can be produced voluntarily, and can also often be suppressed 
by an effort of the will when the act would be attended by pain ; 
but it is essentially a reflex act arising from irritation of nerve 
terminals or trunks, in direct or indirect communication with the 
respiratory centre, principally of the vagus or of the fifth nerve. 
It is designed primarily with the object of removing this irritant 
from the terminals of the pneumogastric in the air passages of the 
lung; but inasmuch as the respiratory centre is incapable of dis- 
tinguishing between an irritant of terminals and one of nerve trunks, 
and between a removable and an irremovable irritant, the act is in 
many cases necessarily ineffectual. We are thus led naturally to a 
division of coughs into (a) coughs useful, {b) coughs useless, the 
former requiring to be helped, the latter to be suppressed as far as 
possible ; and hence our first point in diagnosis is to try to separate 
the two classes. 

First, as regards the sound and features of the cough itself : — 

Cough Useful Cough Useless 

Moist, accompanied by a rattling Dry, barking, or ringing cough, 
or wheezing sound with each characteristically paroxysmal in 

blast ; if at first dry and in- many cases, e.g. whooping cough 

effectual, ultimately results in in later stages ; always ineffec- 

the expulsion of some mucus tual in removing the essential 

or other material from the air cause of irritation. It may re- 

passages more or less propor- suit in the bringing up of a 

tionate to the efforts made. small plug of mucus, but totally 

out of proportion to the efforts 

made. 



5° 



DIFFERENTIAL DIAGNOSIS 



N.B. — In both classes may be included a few unusual or rare 
cases of gross foreign bodies in the tubes, or of the membranous 
casts of plastic bronchitis, in each of which the cough may be dry, 
barky, and severe, or moist and wheezy, but may still result in the 
expulsion of the irritant. 

Now as regards the clinical causation of the two groups. These 
we may tabulate as follows : — 



Cause. 
Disease of external 
ear. 



Elongated uvula. 



Acute pharyngo-ton- 
sillitis. 



Laryngitis, bron- 
chitis, broncho- 
pneumonia, ordi- 
nary pneumonia, 
pleurisy. 



Tuberculosis of 
larynx or of lung. 



Cough Useless 

Principal Diagnostic Points. 

The evidence will be chiefly negative, absence of 
other possible cause for a slight dry cough. 
Under such circumstances it has only to be 
remembered that a foreign body in the ear, or 
a little eczema, may cause such a cough for 
the diagnosis to be suggested, and the sugges- 
tion will lead to a careful examination of the 
part. 

Suspected by the cough and tickling in the throat 
being much worse (possibly only then notice- 
able) on lying down. Absence of thoracic 
signs of disease and presence of the long 
uvula complete the diagnosis. 

Cough (as opposed to mere laboured hawking of 
phlegm) slight, but attended with much pain, 
therefore often suppressed. Condition obvious 
on examination of mouth and pharynx. 

In all these acute inflammatory conditions of the 
air passages the cough is, at least in the earlier 
stages, — say twenty-four to thirty-six hours — of 
the useless type, and may safely be mitigated 
with sedatives ; the temperature, the history, 
and the painful cough are sufficient for a tem- 
porary diagnosis. For a complete one, vide 
under the appropriate subsections (pp. gjeiseq.). 

Both these forms of tubercle, in the stages of 
deposit, before ulceration or suppuration has 
occurred, are associated with a troublesome 
dry cough. In the former additional suspicion 
is aroused by hoarseness or loss of voice, and 
the laryngoscope will clear up the diagnosis. 
For a complete diagnosis of phthisis, vide 
pp. 84 et seq. 



DISEASES OF THORACIC ORGANS 



5i 



Cause. 
Malignant or syphi- 
litic deposit in 
larynx before ul- 
ceration. 



Tumour pressing on 
pneumogastric or 
its branches, or 
on trachea or 
bronchi ; aneur- 
ysm, enlarged 
glands, malignant 
growth. 

Morbus cordis in 
early stages. 



Principal Diagnostic Points. 

Cough and symptoms similar to tubercle, diagnosis 
made with laryngoscope. N.B. — In the later 
ulcerative stages of all these deposits in the 
larynx, though the cough may be in some 
degree useful, it is always persistent and dis- 
tressing to a degree that renders some mitiga- 
tion of it necessary. 

Any of these tumours, in any form, may cause a 
dry, hacking, or brassy cough, which in itself 
should arouse suspicion of some such condition. 
Absence of other obvious cause, and especially 
if combined with paralysis of one or both cords, 
will be the chief diagnostic feature, but vide 
p. 105 for further indications. 

The back pressure of a leaking mitral will, on 
any extra exertion, cause a cough which — at 
first, at any rate — is distressing and useless. 
The diagnosis depends primarily on the presence 
of a bruit. Should this be absent and yet no 
other cause for a cough on exertion be found, 
the consideration of the heart sounds on p. 125 
will be useful. 



Cough Useful 

As remarked above, cough may be looked upon as useful, and 
encouraged accordingly, when it removes irritating material from 
the air passages in something like proportion to its activity and 
force (the force may need reinforcement in the aged or debilitated). 
Hence we find it in — 

The later stages of all acute inflammatory affections of the air 
passages and lungs when secretion has become excessive or suppura- 
tion established, or often enough when the disease has become 
chronic. 

The later stages of phthisis when ulceration and breaking down 
of lung tissue has occurred. 

In bronchiectasis, however arising. 

In some cases of pleuritic effusion or of morbus cordis when it 
would appear that the air tubes are used as the means of carrying 
off excess of fluid. 

In the bursting of abscesses, empyemata, etc., into the tubes. 

The differential diagnosis of these conditions will be the object 



52 DIFFERENTIAL DIAGNOSIS chap. 

of several sections in the succeeding pages. So far as the mere act 
of coughing is concerned, they offer no differentiating points. It is, 
however, worth while to draw attention to the suggestions given by 
the time of day at which a cough is worse. If it is worse at night, 
after the patient has got warm in bed, the suggestion is that it is due 
to some cause other than a mere mechanical stimulus or natural 
secretion, i.e. in an adult suggestive of phthisis or pneumonia, in a 
child of pertussis or bronchopneumonia. On the other hand, if the 
cough is worse during the active working hours or on change of 
atmosphere, this is suggestive of simple catarrh, as in mild bronchitis. 
It is possible that the explanation of this clinical fact may lie in a 
suggestion that the activity of the more virulent microbes is inde- 
pendent of the circumstances of the patient, whether active or 
quiet, asleep or awake, while the milder ones may be more 
dependent on respiratory activity, as we know natural secretions 
are. 

The Sputum as an Aid to Diagnosis 

Sputum is the natural sequel to a useful cough. As a guide to 
the naming of a disease it is not often by its naked-eye characters 
(its microscopical -bacteriological examination is most important) 
of great capital value, but as a guide to the improvement, or the 
reverse, of the condition of our patient's air tubes, during treatment, 
it is of very great significance. It is well to draw the student's and 
young practitioner's attention to the fact that the repeated physical 
examination of the chest which is allowable, and even necessary, in 
hospital work for teaching purposes, is not in private practice 
always advisable ; and many patients will so strongly object to it 
that some other means must be adopted for estimating progress, 
and none are so useful as a few questions on the violence and 
frequency of the cough, and the amount of trouble experienced in 
getting up the phlegm, followed by an ocular and mental inspec- 
tion of the sputum, which should always be kept for the purpose. 

Phlegm, as the natural secretion or excretion of the mucous 
membrane of the air tubes, should be small in quantity, and consist 
merely of almost colourless mucus, with occasional cells and detritus 
of inhaled particles. It is what it should be, in country dwellers and 
non-smokers; but in towns, in smokers and others with dusty occupa- 
tion, it becomes more or less coloured in agreement with these 
factors ; hence black phlegm, unless we see it is due to dark blood, 
need not be a cause for alarm under such circumstances. 



iv DISEASES OF THORACIC ORGANS 53 

In disease the quantity is, as a rule, enormously increased, and 
much besides mucus is present. 

Quantity. — Speaking of quantity only, quite apart from quality, 
it is important to note one point particularly, i.e. whether the 
excess is brought up in large mouthfuls or gulps at a time, with 
quiescence in the somewhat long intervals, or whether it arises from 
an increased frequency in the act of coughing, with but a moderate 
expectoration each time. The former indicates or suggests to us 
that there is a cavity or potential cavity of some kind communicating 
with a bronchus, and emptying itself by cough at intervals ; such 
may be bronchiectasis, or abscess either of lung itself or neighbouring 
organ, or empyema. The latter tends to negative such a suspicion 
if roused by other methods of examination, and suggests instead 
a bronchitis, bronchopneumonia, or ordinary pneumonia, with 
excessive secretion, but without organic dilation of tubes ; the 
absorption of a pleuritic effusion, or the presence of morbus cordis, 
will occasionally very much increase the quantity of sputum. 

Quality. — As regards the quality of the sputum, the following 
are the principal pathological constituents to be found by clinical 
examination : — 

Mucus (excess only is pathological), 

Pus, and nummulation, 

Blood, 

Bile, 

Lung tissue, 

Hydatid hooklets and other parasitic detritus, 

Microbes (particularly of tubercle and actinomycosis), 

Fcetor, 
on each of which I propose to make brief comments. 

Mucus. — As this is the natural secretion of the air tubes, it follows 
that its excess or defect is the pathological phenomenon. In the 
early hours of a catarrh it is defective (hence cough useless and 
sedatives required). Later it becomes excessive but very sticky. This 
excessive stickiness is almost pathognomonic of pneumonia (cough 
still useless, or at least violent and out of proportion to result, and 
to be helped by liquefaction of phlegm). This indicates an acute 
bronchitis or pneumonia. Later still it becomes mixed with pus, and 
looser, indicating that the catarrh has caused suppurative processes 
which, unless very excessive, are known not to be of unfavourable 
omen. 

Pus. — As mentioned above, this is found in the later stages of 



54 DIFFERENTIAL DIAGNOSIS chap. 

all catarrhal affections of the bronchi, and hence, as a rule, is of 
little diagnostic significance ; it causes mucus to assume a 
yellowish or green colouration. There are two conditions of 
suppurative sputum which it is important to bear in mind : (a) 
when the pus comes up very freely and almost pure, i.e. without 
much mucus, rousing suspicion of, or corroborating other indications 
of, the bursting of an abscess or empyema into an air tube, or the 
presence of bronchiectasis ; (b) the condition known as nummula- 
tion of the sputum, in which small masses of pus float quite 
separately and isolated in the spittoon ; it suggests the presence of 
small loculi where the pus can collect before being expectorated ; it 
is seen in its most typical form in, and is very suggestive of, the 
later stages of tubercular destruction ; it is found, but less frequently 
and typically, in pneumonia and bronchitis, especially if some of the 
smaller tubes have dilated. 

Blood. — " Blood-spitting " is a very common complaint, and 
requires considerable care to ascertain its exact source, vide pp. 150 
et seq. Suppose, however, we are satisfied that it arises from some 
pulmonary affection, we have still to consider its significance. It 
may appear in small isolated streaks in the mucus, or clotted and 
free, or it may be more intimately mixed with the sputum, imparting 
a uniform tinge to the excretion. 

If of laryngeal Probably only in streaks or tiny clots, with 

origin. pain in larynx and alteration of tone of 

voice. Unless other source obvious, a laryngeal 

examination must be made, and this will 

clear up the question. 

If tracheal or acute Again probably only in streaks and tiny clots ; 
bronchitis. other signs of tracheitis and bronchitis. 

In chronic bron- Often profuse, condition is fairly obvious in 
chitis. diagnosis, but the occurrence of haemoptysis 

in the disease is frequently forgotten. 

In phthisis. Whether in an early or late stage the haemor- 

rhage may be smart, diagnosis must rest on 
other factors. Apices are especially likely to 
give added physical signs on deep inspira- 
tion. Bacillus, if found, is conclusive. 

In pneumonia. It is especially in pneumonia that the blood 

stains the sputum uniformly. Colour anything 
from mere rusty to dark prune - juice ; the 
darker the worse the prognosis. 

In morbus cordis. Presence of bruits, or, more significantly, other 

signs of cardiac failure, vide p. 124. 



iv DISEASES OF THORACIC ORGANS 55 

In malignant The sputum of patients with recognisable 

disease. malignant disease often contains small masses 

of blood-stained material likened to red- 
currant jelly ; the point may be of importance 
in separating such from other consolidating 
lung trouble {vide p. 105). 

Such are some of the main lines of thought towards a diagnosis 
in cases of pulmonary haemorrhage, but it is easy to see that the 
bleeding itself or its character is of relatively small importance ; 
other factors of much greater weight are involved. 

Bile. — This is but a very rare constituent of sputum, but if 
present is practically pathognomonic of communication between an 
air tube and a pathological excavation of the liver. 

Lung Tissue. — If fragments of elastic tissue are found in the 
expectoration (boiling with caustic potash and examining the 
detritus under the microscope is the simplest plan), the important 
caution is to be sure that what we see has actually come from the 
lung. It is not enough to find elastic fibres, which may have come 
from tiny fragments of food accidentally present ; they must have 
the shape of a more or less open figure 8 indicating their origin 
from the bronchioles or alveoli. If such are present, they prove 
pulmonary ulceration to a demonstration, and render tuberculosis 
almost certain ; doubt can only arise in some few cases of chronic 
disease of the lung, either fibroid pneumonia, or bronchitis with 
associated bronchiectasis. An acute gangrene will reveal itself by 
other more important features. 

Hydatid Hooklets, or other parasitic detritus or eggs, are of course 
immediately pathognomonic of their source. 

Microbes. — The bacilli of tubercle and other bacilli are of course 
equally pathognomonic ; the only cautions are, first, to be sure that 
the staining processes have been properly carried out ; and secondly, 
to remember the difficulty of proving a negative, and so excluding 
tuberculosis too summarily from the absence of bacilli in a few 
fields of the microscope. 

Fcetor. — This proves that the microbes of putrefaction have not 
only reached the dead material of the sputum, but have had time 
to effect their peculiar changes in it ; hence foetor almost certainly 
indicates that the sputum has lain for some time in a potential cavity, 
i.e. a place where such changes could go on undisturbed, or that a 
piece of lung has itself died outright, or some foreign body is 
present in an air tube capable of putrefying ; consequently careful 
search must be made for : — 



5 6 DIFFERENTIAL DIAGNOSIS chap. 

(i) Bronchiectasis. Usuallyassociatedwithchronicbronchitis. Phthisi- 
cal cavities are curiously almost exempt from 
this putrefactive process, though their contents 
have a peculiar mawkish smell very charac- 
teristic. 

(2) Abscess of lung. The main diagnostic features of intrinsic abscess 

Intrinsic or are (a) foetid expectoration, which {b) consists 

bursting into of nearly pure pus, with putrefying detritus, 

lung from with- and (c) the discovery over a localised area of 

in. the lung of pathological physical signs {vide pp. 

64 etseg.). Abscess arising elsewhere and burst- 
ing into the lung will have revealed itself be- 
fore rupture probably. The fcetor (if present) 
and coughing up of quantities of pus merely 
indicate that communication has been estab- 
lished with the air tubes. 

(3) Gangrene. The fcetor of pulmonary gangrene is utterly in- 

describable ; once smelt it cannot be forgotten, 
and when occurring with symptoms of serious 
blood-poisoning leaves no room for doubt or 
error. 

It is well to insert here a caution against mistaking foul breath 
for foetor of sputum ; the latter is only one cause of the former, 
and that a rare one, the nose, mouth, and stomach being far and 
away the most frequent sources of foul breath. 

To sum up the diagnostic value of an examination of the 
sputum, we may say that nearly every disease of the respiratory 
apparatus has, or may have, a form of expectoration which is fairly 
characteristic which, at any rate, lends strong corroboration to 
other physical signs and symptoms, and at times takes a leading 
position as an indicator of the essential condition of the organ — 
improvement or the reverse — under treatment. 

Besides cough and its attendant expectoration, there are one or 
two general alterations in respiratory movements which deserve a 
brief mention and analysis for diagnosis. 

Generally accelerated Respiration. — This, apart from intentional or 
voluntary quickening of the movement, essentially means that the 
supply of oxygen to the tissues is insufficient for their immediate 
(it may be) temporary needs. This may be analysed into : — 

A. Conditions in which an extra supply is required. 
(a) Exertion. A purely healthy and physiological condition, 

exaggerated in convalescence when the tissues 



iv DISEASES OF THORACIC ORGANS 57 

are rebuilding their stable capital of nutritional 
material. 
(b) Pyrexia arising Oxidation is quickened throughout the body. I 
from any dis- have already (p. 35) noticed the importance 

ease. of the temperature-respiration-ratio in draw- 

ing attention to pulmonary complications when 
other complaints of lung trouble by the patient 
are absent. This rule is particularly valuable 
in the specific fevers, when cough may be de- 
liberately suppressed because of the pain it 
causes, or when the patient is too weak to 
cough. 

B. Conditions in which increased frequency of respiratory movement 
is required to keep up the ordinary normal supply. 

(a) Diminished aerat- Seen in bronchitis, pneumonia, emphysema, col- 

ing surface in lapse of lung, phthisis, etc. ; in fact, any disease 

lungs. filling the air tubes or destroying alveoli. 

(b) Diminished or Seen in valvular or muscular disease of the heart, 

obstructed cir- in emphysema, etc. 

culation of 

blood through 

the lungs. 
N.B. — It is probable that these two causes never act absolutely 
independently. Pulmonary disease in itself, e.g. emphysema, invariably 
tends to obstruct the circulation, and cardiac disease tends to fill the 
air tubes. 

(c) Poverty of blood Seen in anaemia, from whatever cause arising. 

in oxygen car- 
riers. 

From the variety and number of the diseases and conditions in 
which increased frequency of respiration occurs, it will be seen that 
the act is in itself not of very great value in differential diagnosis, 
but there are one or two points in it well worth attention : — 

In chronic disease of the lung, e.g. phthisis or bronchitis, the 
patient and his tissues, especially if much wasted, may have got so 
accustomed to the smaller supply of oxygen that shortness of breath 
will not be complained of, and may even be denied, until some extra 
exertion is called for ; whereas in acute disease of the lung the 
shortness of breath is at once obvious, and often very distressing. 

In old people, whose chemical changes are not extremely active, 
very serious lung and pleural trouble may come on extremely in- 
sidiously without any rise of temperature or general discomfort on 



58 DIFFERENTIAL DIAGNOSIS chap. 

the part of the patient, except for a little shortness of breath ; hence 
it is, in such patients, very important to inquire specifically for such 
complaint, and make a careful physical examination of the chest on 
the slightest suspicion. 

In young babies, again, and infants of feeble vitality, slightly 
quickened respiration (it must not be forgotten that their normal 
respiration rate is from 25 to 35), accompanied by a little wheezing, 
may be all the evidence of a bronchitis that is rapidly proceeding 
to become a dangerous and even fatal illness. 

Cheyne-Stokes breathing is a curious variety of respiratory 
movement, in which the patient passes gradually from a condition 
of apncea (which may have lasted some seconds) through a period 
of steadily increasing frequency up to one of very great frequency 
of respiration. It is seen now and again in almost every form of 
disease — uraemia, chronic nervous disease, concussion of brain, 
etc.; its morbid physiology is unknown, and it has no clinical 
diagnostic value ; but it is of very grave prognostic significance, 
few recovering when the condition is well marked as an added 
phenomenon to the symptoms already present indicative of acute 
disease. 

Dyspnoea is a term worth defining, for I find that students so 
frequently use it as the scientific equivalent of shortness of breath. 
It really means difficulty of breathing; no patient ever yet com- 
plained of "dyspnoea," but many complain, and that not indiffer- 
ently, of "shortness of breath," or of "difficulty in breathing," 
terms which are sufficiently explicit in themselves, and should not 
be confounded. My own teaching and practice is to reserve the 
term dyspnoea either for those cases in which the patient complains 
of difficulty in breathing, as, for example, in most cases of asthma, 
or in which we have strong objective evidence of a mechanical 
interference with the free entrance of air to the lungs, e.g. diphther- 
itic membrane, spasm or paralysis of larynx, pressure on the trachea, 
etc. Thus used, the term is of some diagnostic use, indicating one 
of the above conditions as opposed to the numberless causes of 
" shortness of breath." 

Diaphragmatic Breathing. — This is more or less a natural 
phenomenon, in the male sex at any rate, but may become grossly 
exaggerated, and assumes then very grave prognostic significance. 
My own experience of it would compel me to say that it has two 
diagnostic suggestions: (1) that the nervous mechanism of respira- 
tion is gravely interfered with either by gross disease in the thorax, 
or more probably by a serious lesion of the nervous system ; (2) 



iv DISEASES OF THORACIC ORGANS 59 

(a negative inference) that there is no accumulation of fluid in the 
pleural cavity. 

Pressure Effects 

The thorax is certainly not an incompressible cavity like the 
cranium ; its roof, consisting of the dome of the pleura and the 
cervical connective tissue and other soft structures, and its floor, 
viz. the diaphragm, are certainly both easily capable of displace- 
ment or extension ; but the side walls, consisting of sternum, ribs, 
and vertebras, are comparatively inextensible, and the individual 
organs themselves, except the bulk of the heart, are so firmly 
fixed in their places by the mediastinal tissue, that no very great 
addition can be made to the bulk of an intrathoracic organ, and 
no neoplasm can attain any great size without leading to compres- 
sion of some important structure, or to manifest displacement of 
the heart. The gross effects of the pressure or displacement are 
readily enough recognised in most cases, but to estimate exactly 
the diagnostic value of these various pressure effects requires a 
considerable knowledge of morbid-anatomical possibilities and of 
the relative positions of the several structures in the thorax. Into 
these points I do not propose to enter fully, but I wish to give an 
analysis of the principles for completing a diagnosis, leaving the 
application of these principles to be worked out in individual cases. 

We require first, then, a list of classes of structures that may be 
compressed or eroded and destroyed. These comprise : — 

I. Hollow vessels : — Principal Results. 

(a) Lymphatics and CEdema of chest wall or arm. If the thoracic 
thoracic ducts. duct is blocked, chylous ascites is very possibly 

present. 

(b) Veins. CEdema, as in lymphatic block, but the superficial 

veins of the district involved are probably 
also enlarged. 

(c) Arteries. Alteration in the time and volume of the corre- 

sponding pulse felt in an accessible situation. 

(d) Air tubes and Cough with little expectoration, shortness of 
lungs. breath, inspiratory dyspnoea if large tube com- 
pressed, possibly collapse of lung. 

(e) Heart. Displacement of apex beat, possibly unusual 

bruits and altered rhythm. 
(/) (Esophagus. Difficulty in swallowing, or rather feeling of food 

sticking and not reaching the stomach, possibly 
regurgitation. 



6o 



DIFFERENTIAL DIAGNOSIS 



2. Nerves : — 
Of which the most 
important are : — 
(a) Recurrent laryn- 
geal. 

{b) Phrenic. 

(c) Pneumogastric 
and cardiac plex- 
uses. 

(d) Lowest cord of 
brachial plexus. 



Principal Results. 



Spasm or paralysis of vocal cord, hoarseness or 
alteration of voice, possibly dyspnoea and in- 
effectual cough. 

Hiccough or paralysis of diaphragm. 

Disturbance of heart beat, slowing, quickening, 
or irregularity, possibly vomiting. 

Disturbance of function of ulnar and other nerves 
of arm. 



The nature of the nerve disturbances will be better understood 
by reference to p. 315. 

Severe pain in back, worse at night (this is a 
very characteristic feature of bone pain, what- 
ever bone be affected and whatever the cause), 
possibly felt all round the chest from implica- 
tion of intercostal nerves. 

Local pain, and possibly erosion with bulging. 

Visible bulging above clavicle, either persistent 
or on coughing. 

Displacement with easy palpation of liver below 
the ribs, loss of free respiratory movements of 
diaphragm. 



Bones — vertebras, 
ribs, or sternum. 



Roof. 



5. Floor. 



These are the principal results of pressure, 
may be thus tabulated : — 



The chief causes 



obvious on inspection and 



1. Serious deformity The deformity is 
of chest from old palpation, 

spinal caries, 
severe rickets, 
osteomalacia, par- 
alysis, etc. 

N.B. — In a chest seriously deformed by old or recent disease, 
it must be borne in mind that even a slight attack of pulmonary 
disease — pneumonia, bronchitis, etc. — is very apt to prove serious or 
even fatal, owing to the great curtailment of breathing room. This 
is merely an illustration of the great principle of the loss of adapt- 
ability for emergencies or extra work entailed by old structural 
damage, a principle easily remembered in the case of kidneys, 



DISEASES OF THORACIC ORGANS 



61 



livers, etc., but apt to be forgotten for more obvious bodily de- 
formities. 



2. Aneurysm. 



3. Solid growths. 

4. Pleuritic and peri- 
cardial effusion. 



Especially apt to exert pressure on recurrent 
laryngeal and other nerves, trachea, left in- 
nominate vein, and on bone, but vide p. 107 
for further details. 

Press especially on veins (intercostal, azygos, 
etc.) ; vide p. 107. 

Cause displacement of heart and apex beat 
particularly, but vide p. 102. 



Pain in Chest 

Before considering the differential value of a pain in the chest 
it is well to locate the unhappy feeling rather exactly, because 
many people seem to be unaware of the thoracic boundaries, and 
call the abdomen the chest, either out of such ignorance or out of 
modesty. Even when we have located the pain with accuracy, it 
is not always easy to at once fix the offending organ, for some 
abdominal troubles, notoriously dyspepsia {vide below), may cause 
pain referred to the chest, and I have known pleurisy cause such 
extreme abdominal pain as to lead to an erroneous diagnosis of 
peritonitis. 

Chest pain, if due to organic disease situated within the thorax, 
is almost invariably due to one of the following : — 

Traumatism. History obvious. 

Spinal caries. Pain of girdle character and vertebral spines 

tender, possibly also deformed in position. 
Aneurysm. May simulate caries in pain ; vide p. 107. 

Pleurisy. Much worse on deep inspiration, especially on 

coughing ; rub conclusive. 
Pericarditis. Localised in precordial area ; heart beats unusually 

frequent ; rub conclusive, but vide p. 127. 
Heart disease, es- Bruits heard ; pain usually anginal, i.e. very 
pecially aortic. severe tight cramping pain, sudden in onset 

and probably caused by some exertion, though 

this may be only slight. 

Hence we see that even a superficial physical examination is 
not likely to leave us long in doubt about the pain of acute peri- 
tonitis, calculus, or other gross organic disease of abdominal viscera. 
If the physical signs in the chest are not marked, those in the 



62 DIFFERENTIAL DIAGNOSIS chap. 

abdomen are only too obvious. But the relation between cause 
and effect is by no means so easy to trace in the case of pain in 
the chest arising from functional dyspepsia, as mentioned above. 
Such a common correlation is there between heart and stomach 
that it is now a commonplace of medicine to say, " If a patient 
complains of his heart, the first suggestion is that his stomach is out 
of order ; if he complains of his stomach, don't let him go without 
examining his heart carefully." A few leading questions on the 
relationship of the pain to food, to movement, to respiration, will, 
however, tend to clear matters up ; the following points may be 
taken as guides : — 



Pain in Heart Region 



If of Gastric Origin. 

Appears after food, and apparently 
as the direct consequence of its 
ingestion. 

Accompanied by feeling of fulness 
in stomach, often relieved mo- 
mentarily by belching. 

Not increased by walking, which 
is easily possible. 



Heart sounds normal in rhythm 
and character. 



If really Cardiac. 
Appears also quite irrespective of 
whether food be taken or not. 

No such feeling of fulness, not 
relieved by eructation of wind. 

Increased by active movement, 
which may even be impossible 
owing to the severity of the 
pain. 

Probably some cardiac bruit pre- 
sent, or at least alteration in 
rhythm and volume of pulse 
from the normal. 



Notwithstanding these differences, we must not forget that the 
two troubles may coexist ; that, in fact, the heart trouble may be 
producing the dyspepsia, and vice versa, the dyspepsia may produce 
an irritable heart. We must then leave the history and other indi- 
cations to decide which is cause and which effect, a decision all 
the more important as treatment will be founded on it. If the 
heart mischief is primary, there are almost certain to be other 
indications of it — some shortness of breath, oedema of legs, etc. ; 
it is very improbable that dyspepsia will be the only symptom ; per 
contra, if dyspepsia is the primary trouble, there will almost certainly 
be a history of discomfort after meals long antedating the pain in 
the heart. 

There is still one form of pain in the chest which requires 



iv DISEASES OF THORACIC ORGANS 63 

attention from a diagnostic point of view. It is very common in 
my experience, situated about the lower ribs on either side, but 
very much more common on the left. It derives its interest from 
the entire absence of any physical sign to account for it ; no heart 
disease, no friction sounds, tongue clean, bowels regular, and no 
discomfort after meals. A stitch in the side from excessive 
exertion or laughter, etc., is a common phenomenon, due probably 
to cramp of one or two intercostal or abdominal muscles or 
segments ; intercostal neuralgia, too, of a typical darting character 
I have heard of and read of, but seldom seen : but the pain to 
which I refer does not agree with either of these. It is constantly 
present more or less, but is much increased by coughing or violent 
respiratory movements, and remains fixed in its original situation. 
I do not say that I can point to the cause of all such pains, but I 
would draw attention to what I believe to be the explanation of 
many of the cases. 

Nothing is commoner on post-mortem examination than to find, 
besides the definite disease which has caused death, one or more 
of the following distinctly pathological conditions, evidence of past 
local trouble, viz. : — 

1. Adhesions of lung to dia- Diaphragmatic pleurisy, 
phragm. 

2. Adhesions of spleen to dia- Perisplenitis, 
phragm. 

3. Adhesions of spleen to intes- Perisplenitis, 
tine. 

4. Adhesions of intestine to gall Local peritonitis, 
bladder and liver. 

5. Adhesions of liver to dia- Perihepatitis, 
phragm. 

6. Thickenings of splenic capsule. Fibrous and even calcareous. 

The argument in regard to such post-mortem findings runs 
thus : — 

1. They are definite and indisputable evidence of old local 
trouble. 

2. They offer no suggestion that the trouble was of a disabling 
character, or so severe as to necessitate, or perhaps even suggest, 
confinement to bed ; and hence they are easily forgotten afterwards. 

3. When recent, they were in all probability associated with 
pain, and even as old pathological adhesions they probably cause 



64 DIFFERENTIAL DIAGNOSIS chap. 

pain by restriction of the natural movement, which would follow 
ordinary energising of abdominal and thoracic muscles, i.e. at- 
tempted movement. 

4. The pain would probably be fixed in position about the 
lower ribs, quite likely be made worse by extra movement, as of 
cough, or even by the digestive movements or physiological con- 
gestion of the stomach and intestine — in fact, just such a pain as 
we are discussing. 

5. From their position, and from the little movement-in-contact 
of organs concerned, they would be unlikely to give rise to an 
audible rub or other objective physical sign. 

On the other hand, I am obliged to state that I am unable to 
say definitely that these persons had suffered from our present form 
of pain, nor can I say that they had not a definite disabling 
illness which might have resulted in such adhesions and thicken- 
ings. On the whole, I am inclined to think that the appearances 
are too common in proportion to histories of severe illnesses, and 
that they do explain most satisfactorily the pain under discussion. 

PHYSICAL SIGNS OF THORACIC DISEASE 

As with the symptoms, so with the physical signs of intra- 
thoracic disease. I do not propose to go systematically through 
each and all, but merely to touch on those points which are of 
special diagnostic value, or on which, experience in teaching has 
shown me, the ordinary text-books hardly lay sufficient stress. 

Comparison of the Two Sides 

It cannot be too much insisted upon that the thorax in each 
and every individual is a closed box — a drum, in fact — with its 
own amount of external covering or damper of vibration, its own 
individual shape and build — in fine, its own complete group of 
special peculiarities ; conrequently it is impossible to lay down any 
law as to what should constitute its normal shape, or the normal 
sound elicited by striking it. There is no such thing as an absolute 
guide to discriminate the normal from the abnormal ; that which 
would be natural in the chest of a healthy, stout woman, or in a 
baby, or even in an old deformed chest, would be distinctly patho- 
logical in the chest of a thin man, an adult, or in a well-formed 
chest. Our only reliable guide, then, is a comparison of the two 



iv DISEASES OF THORACIC ORGANS 65 

sides of the same chest, combined with experience of average chests ; 
and be it remembered that the two sides must be examined and 
compared at corresponding points and in a similar manner. It is 
no good comparing any of the physical signs, seen, felt, or heard, 
of the front or axiliary region of one side with those of the back or 
suprascapular region of the other, nor is it any good to lay the 
pleximeter finger along the ribs and spaces in one case, and across 
them in another. Thus compared, a little swelling or oedema on 
one side only, a little difference in movement, in tactile vocal 
fremitus, in dulness on percussion, and especially in loudness and 
distinctness of breath and voice sounds acquires an enormous 
increase in importance from what it would have if the (possibly) 
pathological change were found on both sides to the same degree. 
In one case disease past or present is there ; in the other we are 
probably dealing with a natural, if not healthy (as in old deformity), 
condition. Never examine one side of a chest only, however obtrusive 
be the local complaint of the patient ; compare, compare, compare I ! 

Physical Signs give Physical Conditions only 

This limitation in the diagnostic utility of the physical examina- 
tion of the chest is too apt to be lost sight of, and deserves 
emphasis. It enables us to see a bulging and motionless chest, 
but it does not decide the reason for this. It proves the presence 
of undue secretion in the air tubes, but it does not give us the 
tubercle bacilli which may be causing it. Dulness on percussion 
does not decide between serum, blood, and pus ; and external 
signs of internal pressure leave aneurysm or malignant growth still 
in doubt. Bearing this limitation in mind, we may proceed to 
consider what can be learnt by it. 

Inspection 

The principal points noticed on inspection, and their pre- 
liminary indications, may be thus sketched out : — 

Old or permanent Probably symmetrical, and causing forward pro- 
deformity. Passed jection of sternum, or, per contra, considerable 
rickets. depression of sternum and costal cartilages. 

Old spinal curvature. Probably asymmetrical, hump on back, and 

twisting on vertebral axis. 
Emphysema. Rounded, barrel-shaped chest, with but little re- 

spiratory movement. 
F 



66 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



N.B. — All three will possibly, and even almost certainly, materially 
alter the results of percussion and auscultation, owing to changes of 
position in the organs and alteration in lung structure. 

Recent bulging of Suggests a large accumulation of fluid in pleura, 

one side. or a new growth. Measure the two sides to 

see if the increased size of one is real, or 

apparent only. Look for oedema of one side 

or anything like a local bulging or pointing. 

Fat or thin chest. Remember fat is a bad conductor of any vibra- 

tions ; the condition is obvious enough in 
itself, but must be remembered in listening to 
or percussing the chest. 

Enlarged veins. An important sign of obstruction to the venous 

return of blood. If due to cardiac disease or 
to generalised lung mischief, it will be noticed 
chiefly in the neck, jugulars, etc. ; if due to a 
local pressure (aneurysm or growth), more 
likely in the walls of the chest, or arms, and, 
possibly, abdomen. 

(Edema. If confined to one arm or one side of the 

chest, it is very strongly suggestive of a 
malignant growth with much local pressure. 
If general, more likely to be only part of a 
renal or cardiac dropsy. 

Local tumour. If only connected with skin or muscles, belongs 

to the domain of surgery. If evidently coming 
from within the thorax, may be a malignant 
growth, an aneurysm, or a pointing empyema. 



Palpation 
By feeling the chest we shall perceive : — 



(Edema. 



Tactile vocal fremitus is increased 
by anything which allows of a 
freer vibration of the chest wall 
in response to the vibrations of 
the voice, hence noted in — 



Already seen by inspection, but its 
limits are best ascertained by 
the present method of examina- 
tion. 

(a) Thin chests, or in parts of the 
chest least covered. 

(6) More powerful voice of a man, 
and in deeper tones. 

(c) Consolidation of the lung, of 
whatever nature, provided that it 
still remains in immediate con- 
tact with the chest wall. 



DISEASES OF THORACIC ORGANS 



67 



Is diminished, per contra, by any- 
thing that damps off the vibra- 
tions. 



Position of heart's apex beat. 



Thrill of heart beat. 



(d) Occasionally by very large effu- 
sions into the pleura completely 
compressing the whole lung. 

(a) Fat chests and parts well 
covered either by fat or muscle. 

(6) Less powerful voice vibrations 
in women and children, and 
higher tones. 

(c) Separation of the lung from 
the chest wall by fluid collections. 

(d) Growths of parietal pleura not 
involving visceral layer or lung. 

Vide pp. 123 and 133. Not felt in 
fat people very often, nor in 
emphysema. Fluid effusions in 
pleura are the great cause of 
displacement. 

Vide p. 114. 



Percussion 

By percussion we estimate the relative degrees of resiliency or 
elasticity of the chest wall, and get a note varying in tone and 
quality from hyper-resonance to complete dulness. 

Resiliency or elasticity of wall can only be properly appreciated 
when the finger is used as the pleximeter (hence the absolute objec- 
tion to the use of all artificial pleximeters of any material), and a 
knowledge of its varying degrees in deformed chests and in health, 
its absence or presence with associated signs in disease, can only be 
gained by experience ; it cannot be communicated by writing, but 
once acquired its value is very great. We may classify its essential 
features as under, with their indications : — 



Its complete pre- 
sence with ordin- 
ary but varying 
degrees of reson- 
ance. 



Its presence with a 
note known as 
dull gives an im- 



Indicates that the parietal pleura is practically 
healthy, free from any degree of deposit or 
growth, and not thickened to any great extent, 
though it may be adherent to the visceral 
layer ; and that there is no extensive pleural 
effusion. Pneumothorax, emphysema, or 
bronchitis and other lung conditions are not 
thereby excluded. 

This is found in pneumonia and other conditions 
of consolidation of the lung, provided that it is 
not separated from the chest wall by fluid, and 



68 DIFFERENTIAL DIAGNOSIS chap. 

pression as though that the parietal pleura is not much implicated. 
one were percus- This is the special utility of the phenomenon, 
sing a thick piece viz. to decide as to whether a pneumonia is or 
of wood — a wood- is not accompanied by much pleural effusion, 
eny tone. The exploring needle is the only other method 
of determining the point. 
Its absence with a This indicates a pleural effusion of considerable 
note known as extent, or a marked thickening of the pleura, 
dull gives an im- but — N.B. — // does not give the reason for the 
pression as though effusio?i or thicke?ring, a new growth, recent in- 
one were percus- fa/nmation, or long antecedent disease. 
sing a brick wall 
or the thigh, and 
renders the dul- 
ness absolute. 

It will be noticed that these indications are directed almost 
entirely to the condition of the pleura, or to the introduction of 
considerable consolidation of the lung. The reason for this is in 
general terms easy to see, viz. the elasticity, and, I may say, the note 
elicited, depend entirely on the capability of the part struck to 
vibrate. This capability is fixed primarily by the shape (including 
old deformity now become the original shape), structure, etc., of the 
chest {vide supra), and is diminished (or increased) more by an altera- 
tion in the pleura and its contents, e.g. fluid (or air-increase) and 
introduction of considerable underlying solidification, than by any- 
thing else. 

Note elicited apart from Resiliency of Wall. — To explain accurately 
the variations in this note is not so easy as the explanation of the 
variations in general elasticity of the chest wall, but it seems fairly 
obvious that if a certain combination of healthy lung, pleura, and 
other structures, including the chest wall, gives in response to a blow 
a certain note, then an alteration in any of these organs or condi- 
tions should alter the note at the spot where the alteration exists. If 
this be not an entirely satisfactory scientific explanation, it is, at any 
rate, the expression of a clinical fact learnt by experience ; and hence 
the incalculable importance of comparing the two sides of the chest 
for detecting mischief on one side only. We must not forget, how- 
ever, in this comparison, the asymmetrical position of the organs in 
the chest, the heart on the left, the liver below on the right, and 
the peculiar course of the aorta, with asymmetry of its main trunks. 
It is not worth while to attempt to tabulate the clinical causes that 
may produce alterations in the percussion note, but attention may 



iv DISEASES OF THORACIC ORGANS 69 

be drawn to the paragraphs on the diagnosis of early phthisis, 
pneumothorax, excavation of lung, etc. 



Auscultation 

By the application of the ear (immediate) or of some form of 
stethoscope (mediate auscultation) to the chest, we try to appreciate, 
and then estimate the meaning of, any sounds which are produced 
by the natural movements of respiration and circulation ; or we 
apply artificial means such as tapping or shaking for the same pur- 
poses. These sounds may be subdivided in their origin into : — 

A. Those arising in and transmitted through the air tubes, 
including — 

(1) The natural sounds of the passage of the respired air. 

(2) Adventitious, or sounds added on to these natural ones, 

but still simply respiratory in causation. 

(3) The sounds produced by the voice. 

B. Those arising from pathological conditions of the pleura : — 

Friction sounds. 
Creaking. 

C. Sounds produced artificially by tapping the chest, and succus- 



D. Produced by the circulatory apparatus. Vide subsequent 
section. 

As regards their characters and meanings, we may classify them 
as follows : — 



A. ( 1 ) Natural Breath Sounds 

Point where heard. Normal sounds. Significance. 

Over larynx and Inspiration and expira- In laryngeal obstruc- 

trachea. tion, distinctly a tion stridor and 

noisy, non- musical hoarseness may be 

rush of air, and detected. 

both equally so = 

tracheal breathing. 



7° 



DIFFERENTIAL DIAGNOSIS 



Point where heard. 
Over larger bronchi, 
e.g. interscapular 
space or R. sterno 
clavicular articula- 
tion. 



Over ordinary lung 
tissue. 



Normal sounds. 
Inspiration louder 

than expiration, but 
the latter very dis- 
tinct and audible = 
bronchial or tubular 
breathing. 



Inspiration distinct, 
ending in or con- 
stituting vesicular 
murmur ; expiration 
scarcely or not at 
all heard. 



Significance. 

Has no abnormality in 
itself, only becomes 
abnormal by — 

(a) Being heard in the 
wrong place = too 
free conduction 

through solid lung 
or dilated tube. 

(£) Not being heard 
in the right place 
from compression of 
a tube, etc. 

Its absence is certainly 
abnormal, e.g. over 
lung solidified by any 
cause. In babies, 
in unusually thin 
adults, and in one 
lung which is doing 
the work of two, 
the vesicular mur- 
mur is undoubtedly 
exaggerated, and 
constitutes the harsh 
breathing of some 
authors. 1 



(2) Additional or Adventitious Sounds are in their nature essentially 
pathological, so we have only to discuss their variations and mean- 
ing. They may be subdivided as follows : — 

I. Interrupted : 2 

1. Fine sounds (crepitations) are such as would be pro- 
duced by the separation of two sticky surfaces, that 

1 Some authorities on auscultation will not admit the use of the term " harsh 
breathing," but I must say I know of no other term that can better describe the sounds 
heard in the three conditions mentioned above. 

2 By thus strictly defining the terms "crepitations" and "rales" according to 
the time in the respiratory cycle in which they are heard, it seems to me that they 
gain in accuracy for use, and indeed also in meaning and significance. The adjectives 
" coarse " and " fine " may still be used for either, occurring in its proper time ; and 
from the coarseness or the reverse, and from the time definition, we may form a tolerably 
accurate opinion of either (1) the probable size of the tube in which the sound arises ; 
(2) whether the air has an actual thoroughfare through the tube, or only goes into and 
back again out of it ; (3) the state of the secretion, the more liquid, the coarser the 



DISEASES OF THORACIC ORGANS 



7i 



is, in fact, the actual cause of them, and their place of 
origin is the alveoli and very finest air tubes of the 
lung. They are heard during inspiration only. 
2. Coarser sounds and moister (rales) are produced by the 
passage of air through a more or less viscid secretion, 
and represent the bursting of air bubbles in the fluid ; 
they are produced in all tubes larger chan those 
causing crepitations only by the passage of air 
through the secretion. They are heard therefore during 
both expiration and inspiration. 

II. Continuous sounds : 

These are the equivalent of the term rhonchus as used 
by the late Dr. Fagge, the main point of the defini- 
tion consisting in the sound remaining at a certain 
level or pitch, possessing, in fact, a certain musical 
tone and quality throughout inspiration or expiration, 
or both. Of the sounds themselves there are many 
varieties : whistling, cooing, snoring, etc., according 
to the depth of tone or originality of term-invention 
of the listener. They are produced by secretion 
adhering in local masses to the wall of a larger tube, 
thus forming a sudden and adventitious narrowing of 
the lumen round which the air passes with a musical 
note. 



(For Tactile Vocal Fremitus vide under 



(3) Voice Sounds. 
Palpation.) 

Normally. Abnormally. 

Over trachea and Loud and fairly dis- Hoarseness the only 
larynx. tinct. detectable variation, 

owing to irregular 
growths or secretion 
covering the cords. 
Over larger bronchi. Not so loud, and more No idiopathic abnor- 
indistinct. mality, only abnor- 

mal like the breath 
sounds by hetero- 
topy. 

sound, and the more likely, in the finer tubes, to allow air to actually bubble through 
it both ways. The two may both occur in the same breath consecutively to one 
another, a circumstance which would strongly suggest that an alveolar or capillary 
affection were supervening on a catarrh of the larger tubes, a most useful danger 
signal, therefore. 



72 DIFFERENTIAL DIAGNOSIS chap. 

Normally. Abnormally. 

Over lung tissue. Mere confused mur- Increase of spoken 

mur or not at all. words (broncho- 

phony) denotes a 
pathological, in- 
creased facility for 
transmission from 
the larynx (solidifi- 
cation of structure, 
dilated or ruptured 
tube, cavity, etc.). 
Increase in whispered 
words (pectoriloquy) 
denotes still greater 
facilities for sound 
transmission from 
the larynx. Altered 
sound of voice, only 
one noticeable form 
(aegophony), a pecu- 
liar bleating tone 
strongly character- 
istic, if not patho- 
gnomonic, of pleural 
effusion. 

In addition to the above classes of regular voice and breath 
sounds, we must notice one or two important modifications of them. 

Cavernous Breathing is primarily an exaggeration in loudness of 
tubular breathing, but it has in addition a musical character of its 
own — comparable to the notes produced by blowing over the 
mouth of an empty bottle, and due to the same essential cause, 
viz. interfering currents of air echoing in a hollow. When heard 
in typical form this cavernous breathing is characteristic of a cavity, 
pulmonary or pleural, communicating freely with a tolerably large 
bronchial tube. 

Tinkling Sounds produced by the falling of drops into the body 
of a liquid contained in a resonating chamber ; hence they are only 
heard when the liquid has been violently driven over the surface 
of either a pulmonary or pleural cavity by coughing or succussion. 

Cogwheel Respiration is a peculiar form of interrupted inspiration, 
as though the air entered in a series of little jerks. It is almost con- 
fined in its appearance to the upper lobes of the lungs, and was 
formerly thought to have much, now only a very little, significance 



iv DISEASES OF THORACIC ORGANS 73 

as indicating early stages of phthisis, causing unequal difficulty of 
air entrance into certain lobules. My own experience would lead 
me to say that it is frequently met with in perfectly healthy lungs, 
and that its chief significance is a very minor one, viz. that the 
patient is nervous, and totally unaccustomed to breathe by in- 
tentional or voluntary movements. 

B. Pleural Friction Sounds are well known, to-and-fro rubbing 
sounds. There are only two sources of difficulty in their diagnosis : 
the one is to separate them from fine crepitations, and the other 
from pericardial friction ; the latter is identical in character. From 
the former they are separable by being coarser, and sounding more 
immediately in contact with the stethoscope, but principally and 
essentially by being heard both with expiration and inspiration ; 
a doubtful sound heard with both movements must be either a rub 
or rales, and the latter will be evidently bubbling. The need for 
separating them from pericardial friction sounds arises only in the 
neighbourhood of the pericardium, and there the simple manoeuvre 
of listening while the patient holds his breath will usually be suffi- 
cient, pleural sounds then of course ceasing, except in the occasional 
cases when pleuro-pericardial adhesions exist, and then the import- 
ant diagnostic point is to recognise by the continuance of the sound 
during the cardiac cycle that the pericardium is affected. 

Pleural Creeks are rare, and only heard in exceptional cases of 
very old-standing chronic dry pleurisy. 

C. Sounds heard by Tapping the Chest and by Succussion. — These 
include : — 

Bell Sound, the ringing echo across a chest produced by laying 
one coin on the wall and striking this with another coin. The 
necessary condition for its production is a fairly large empty space, 
and hence it is useful in detecting a pneumothorax, and its presence 
may be corroborative of other evidence of a pulmonary cavity. 

Splashing Sounds produced by shaking the patient ; can be but 
seldom required, but indicate, when heard, air and fluid in the 
pleura. 

This classification gives in a fairly comprehensive and com- 
prehensible manner the chief ordinary pathological sounds heard 
in the thorax. For these abnormalities of natural phenomena my 
chief aim has been to indicate the principles and reasons which, 
when well grasped, will give a rational foundation for explaining any 
others that may be found in a given case. In practice the difficulty 
is not so much to hear and understand the physical meaning of 



74 DIFFERENTIAL DIAGNOSIS chap. 

intrathoracic sounds, as to know what name others have given to 
the sounds we hear, and thus to avoid serious misunderstandings 
and confusions of nomenclature. Tubular and bronchial breathing, 
harsh breathing, rales and rhonchi and crepitations are illustrations 
of disputed points in affixing labels to aural perceptions. I here 
assume tubular as identical with bronchial breathing, and shall 
endeavour in the succeeding paragraphs to follow my own defini- 
tions of the remaining sounds. 

Having thus cleared a good deal of the ground of symptoms 
and physical signs, we will now proceed to discuss some of the 
diseases on which the phenomena depend. 



LARYNGEAL AFFECTIONS 

The symptoms that are likely to call attention to the larynx as 
the seat of disease are : — 

(i) Pain felt locally. 

(2) Cough, at first almost certainly useless, and only later, if 

ever, useful, i.e. with equivalent expectoration. 

(3) Especially a combination of (1) and (2). 

(4) Alterations in voice, hoarseness, huskiness, aphonia, etc. 

N.B. — In one great and dangerous group of laryngeal affec- 
tions, viz. paralysis of abductors from disease at a distance, there 
are very often no symptoms whatever (if a possible slight shortness 
of breath be excepted), and the condition is only discovered by 
laryngoscopic examination, either as a routine matter or because 
other features of the patient's complaints have suggested that a 
paralysis might be found. 

The causes to which those symptoms may be due are inflam- 
mation, acute and chronic, new growths, and paralysis of laryngeal 
muscles. To endeavour to associate symptoms with causes and to 
make an exact diagnosis without a laryngoscopic examination is 
simply to attempt the impossible, and in what follows the final 
necessity of such examination must always be assumed, though a 
strong degree of probability may certainly be arrived at by a fair 
consideration of the history and circumstances of the case. 

Hoarseness of voice, if it occurs in a child, is almost certainly due 
to either acute laryngitis (simple or membranous) or to papillo- 
mata of the cords. Ulcers of syphilitic, tubercular, or malignant 
nature are practically unknown in childhood, and so is paralysis 



DISEASES OF THORACIC ORGANS 



75 



of the cords, except post - diphtheric, and then the history is 
tolerably obvious on slight inquiry. The acute pyrexial illness with 
catarrh and obvious faucial congestion will easily decide that acute 
laryngitis is present, but only the laryngoscope will prove that there 
is or is not also a papillomatous condition, or show a case of pure 
and primary false membrane of the larynx. In adults the same 
hoarseness of voice may have the ulcers above mentioned as addi- 
tional causes, but not every conjunction of apical phthisis with 
hoarseness, of gumma of the liver, with the same voice disturbance, 
has distinct ulceration of the cords as the necessary and sole cause 
of this latter symptom. Phthisical and syphilitic patients are not 
exempted from a simple laryngeal catarrh. 

The following table gives the main points of distinction between 
the various forms of — 



Ulcers of the Larynx 



Tubercular. 

Slow in progress, and 
not much destruc- 
tion till a long in- 
terval has passed. 

Shallow, superficial 
ulcers, without much 
swelling or infiltra- 
tion. 



Curiously painful on 
swallowing ; com- 
moner from say 
twenty to forty-five 
years. 

Almost certainly evi- 
dence of pulmonary 
infection of tubercle, 
of chronic type. 

Cords freely movable. 



Syphilitic. 

Rapid in extension 
when once broken 
down. 

Deep, ragged, sloughy 
ulcers, with much 
tumefaction. 



Little painful ; com- 
moner from say 
thirty-five to fifty. 



Pulmonary association 
of a chronic type ; 
very rare ; may be 
septic aspiration- 
pneumonia. 

Cords not so free. 



Malignant. 

Intermediate in rapid- 
ity. 



Ulcer itself not very 
deep, but much ex- 
cess of tissue for- 
mation, and not 
much simple swell- 
ing. 

Little painful ; com- 
moner over fifty. 



If lungs affected at 
all it is with acute 
septic bronchopneu- 
monia. (Schluck- 
ungs-pneumonie.) 

Cords often quite fixed 
and immovable. 



76 



DIFFERENTIAL DIAGNOSIS 



Laryngeal Paralyses 

The functions of the larynx with its vocal cords are three. 
These, with their natural nerves and muscles, may be thus tabu- 
lated : — 



Function. 


Action of Cords. 


Muscles. 


Nerve. 


Speech 


Approximated 


Arytenoids, lateral 


Recurrent 






crico-arytenoids 


laryngeal. 




Made tense with 


Crico-thyroid 


Superior 




varying tension 




laryngeal. 




' in voice expres- 








sion 






Cough (or extra- 


First opened by 


Posterior 1 cricoaryte- 


Recurrent 


ordinary res- 




noid 


laryngeal. 


piration) 


then firmly closed by 
then suddenly 


All the other muscles 






opened by 


Force of air and re- 
laxation of adductor 
muscles. Possibly by 
action of posterior 
crico-arytenoid 




Ordinary breath- 


Very little move- 


Slight abduction in in- 


Recurrent 


ing 


ment, but what 


spiration ? Slight 


laryngeal. 




there is tends to 


adduction in expira- 






allow free 


tion ? ( No movement 






entrance, with 


according to Semon) 






gradual exit of air 







We should naturally expect, then, that paralysis of muscles should 
interfere with some or all of these functions. In the main the in- 
ference is correct, but the exceptions are very important. The 
affection may be uni- or bi-lateral : it may be of adductors or abduc- 
tors, or both. The results, with their reasons, are as follows : — 



Unilateral Abductor Paralysis 

Speech. Very little or not at all affected, because (i) the 

cords can still approximate ; (2) they can still 
be made tense by the crico-thyroid. 

1 Even for a student fairly well up in anatomy it may be a little difficult to 
remember the action of the laryngeal muscles, The O in posterior may help him to 
remember that this is the only muscle which always and consistently Opens the 
larynx. 



IV 



DISEASES OF THORACIC ORGANS 



77 



Cough, or extra- 
ordinary respira- 
tion. 



Respiration. 



In the later phases of the act unaffected ; same 
reasons as for speech. In its first violent in- 
spiration possibly a little difficulty or stridor, 
because extraordinary inspiration requires the 
larynx to be as widely open as possible. 

Ordinary, unaffected, because the slight respira- 
tory movement can easily be affected, by the 
other cord. 



Bilateral Abductor Paralysis 

Speech. Still frequently unaffected. Reasons under Uni- 

lateral Paralysis. 

Cough. In later stages of the act unaffected, because — 

reasons above. In violent inspiratory phase 
probably considerable difficulty or stridor, 
because the lax cords may be drawn together 
by the draught of air, and completely close or 
seriously narrow the aperture of entrance. 

Respiration. Ordinary, probably unaffected, but may be occa- 

sional severe dyspnoea. Reasons under In- 
spiration of Cough. 

Unilateral Adductor Paralysis 

Speech. Probably unaffected, because the tensor is still 

sufficient to put the cord in a vibratory condi- 
tion. Hence a further deduction may be made, 
that if the voice is altered, and only unilateral 
adductor paralysis seen, the probabilities are in 
favour of a source for the paralysis high up, 
before the superior laryngeal nerve is given off. 

Cough. In later explosive phase probably weakened, 

because the air begins to escape past the lax 
cord as soon as pressure increases in the ex- 
piratory effort. Extraordinary inspiration 
unaffected. 

Respiration. Unaffected to any appreciable degree, because air 

can get freely in, and the exit aperture is so 
little increased. 

Bilateral Adductor Paralysis 

Speech. Even now may be unaffected materially except 

for shortness of breath through loss of expira- 
tory control, because — vide argument above in 
unilateral trouble, which still holds good. 



78 DIFFERENTIAL DIAGNOSIS chap. 

Cough. Later explosive stage almost nugatory, because 

air now escapes very freely directly any excess 
of pressure behind is produced by expiration. 
Extraordinary inspiration unaffected ; aperture 
of entrance very free. 

Respiration. Probably a little quickening of respiration, because 

of the loss of control over expiration, so that 
air escapes too freely. 



Speech. 



Cough. 
Respiration. 



Total Laryngeal Paralysis 

May even now be nearly perfect as regards tone, 
but shortness of breath will be noted in con- 
tinuous speaking, because — if the tensors have 
escaped they are still sufficient, or nearly so, 
for tone in single words, but adductor paralysis 
will cause shortness of breath {vide above). 
If voice is quite lost, and tensors also para- 
lysed, we are justified in diagnosing a central 
lesion in the medulla affecting both roots. 

Non-explosive and nugatory, because of adductor 
paralysis. Inspiratory phase, possibly dyspnoea 
and stridor, because of adductor paralysis. 

Ordinary, as in all the others may still be unaf- 
fected for the reasons above. 



N.B. — An opposite and complementary line of reasoning may 
be applied to spasms of the larynx, which are much rarer and only 
in laryngismus stridulus seen to perfection. 

Into the actual causes of these paralyses I do not propose to go 
very deeply here ; a few will be noted below under Tumours of the 
Thorax, and the subject will be apparent again in the nervous 
section. The following outline classification is, however, useful ; 
it is mainly after Sir F. Semon (B. M. J., January i, 1898), but 
rearranged : — 



Functional. 



Toxaemia 



So-called hysterical. 



Lead, arsenic, and 
possibly other 

metals. Diphtheria, 
typhoid, rheuma- 
tism, etc. 



DISEASES OF THORACIC ORGANS 



79 



Organic. 



Primary disturbance in 
the central cells of< 
medulla or cord. 



' Bulbar paralysis. 

Tabes dorsalis. 

Disseminated scle- 
rosis. 

Haemorrhage. 

Softening. Tumours 
of medulla. 



Primary disturbance in . 
the nerve trunk. ' 



Such cases of 
toxic group 



Traumatism. 



the 
as 

have ended in per- 
manent destruc- 
tion. 

Pressure of aneur- 
ysms, malignant 
tumours, inflam- 
matory thickening 
(pleural, pericar- 
dial, meningeal). 

Syphilitic processes 
similarly situated 
to inflammation. 

f Surgical. 
J Suicidal. 
1 Accidental. 
Homicidal. 



The point of greatest practical importance is to determine 
whether a given paralysis is organic in origin, with practically no 
chance, or functional, with a fair chance, of recovery. For the 
toxaemic group of functional cases the great point is to be aware 
of their existence, and should paralysis be discovered a history of 
previous or coexistent illness must be carefully inquired for, and its 
possible treatment by metallic drugs investigated. The affection 
itself has no distinguishing features, though it may be expected to 
be of a bilateral type owing to its origin in circulating toxins. 

For the so-called hysterical paralyses the following points are 
probably sufficient : — 

i. The patient will come with a predominant complaint of 
loss of voice. 

2. Close physical examination will reveal no gross organic 
lesion, but will probably show — 



8o DIFFERENTIAL DIAGNOSIS chap. 

3. Other features of nervous instability. 

4. The sex will probably be female. 

5. The age will usually be under thirty. 

6. The type of paralysis will be adductor and tensor, the 
combination of the two indicating a cerebral origin, which this 
undoubtedly owns. 

As no danger (of asphyxia at least) can arise from adductor 
paralysis, vide table for reasons, the mental association of this form 
with the usually good prognosis in hysteria may help the student 
to remember the clinical fact that by far the majority of cases of 
adductor paralysis are functional, while a much greater proportion — 
in fact, all cases of abductor paralysis — are of grave and probably 
very serious import. 

PNEUMOTHORAX 

Is a condition in which air in the sac separates the two layers 
of the pleura ; this may occur either over the greater part or whole 
of the lung, or over much smaller areas limited by previous ad- 
hesions. It is a condition easily liable to be overlooked or mis- 
understood, and yet of frequent occurrence, so that it is well we 
should understand the principles of its natural history and 
mechanism, which are not, I think, sufficiently clearly set forth 
in most text-books. 

In origin, then, the gas must be : — 

1. Admitted from without. Traumatism. 

Surgical procedures. 
External fistula opening into sac 
(rare). 

2. Developed in situ. From decomposition of a pleural 

effusion (also rare). 

3. Admitted from within. (Esophagus (cancer, etc.) j £ 

(a) Bursting of a gas-holding Stomach (ulcer, cancer, etc.) -| 2 
viscus or cavity other than Subdiaphragmatic abscess. 3 
pulmonary. ^ 

(b) Laceration of visceral pleura Phthisis (most commonly), 
and lung. Abscess or gangrene. 

Emphysema. 

Violent respiratory efforts in healthy 

lungs (very rare). 
Penetration of broken bone through 

pleura. 



iv DISEASES OF THORACIC ORGANS 81 

Admitting that the condition exists, the diagnosis of the source, 
according to the above table, presents but few difficulties. In the 
first group, "Admitted from without," both the cause and the 
condition are obvious, and require no discussion. In the second 
group, " Developed in situ" the pleural effusion will probably have 
already attracted attention ; the smell of a little fluid withdrawn by 
aspiration will leave no doubt about decomposition : such cases 
are, however, extremely rare, and our further analysis will be partly 
applicable to them. In group 3 (a) the previous symptoms will prob- 
ably have made the source clear if the pneumothorax be discovered, 
as, indeed, they will also probably have done in group 3 (b), but it is 
especially to this last group that our argumentative analysis applies 
for the estimation of the occurrence of the accident. 

We must first claim one or two postulates which are, I think, 
justifiable :— 

Postulate 1. That the pleura must be healthy (or at least not 

adherent). Over the area of separation this must be true, 

except under conditions of gaseous pressure too high to 

take into clinical consideration. 
Postulate 2. If the pleura be healthy or non-adherent, the 

admission of air to its cavity must allow of some collapse 

of the underlying portion of the lung. 
Postulate 3. This collapse must diminish (it may be in slight 

degree) the utility of the affected lung. 
Postulate 4. Laceration of healthy pleura must be attended by 

some pain if consciousness is still present. 
Postulate 5. (Not quite so obvious, but justified, I believe, by 

post-mortem experience.) The opening into the pleura 

must be (a) a round hole; or (b) a valvular rent;, or (c) a 

slit more or less irregular. 
Postulate 6. That the admission to the healthy pleura of air or any 

foreign material will cause cough of greater or less severity. 

Granted these postulates, we may divide the immediate 
symptoms of the occurrence of pneumothorax into the inevitable or 
constant, and the quasi-accidental or variable. 

The Inevitable or Constant are : — 

1. Cough. — This is, in fact, the actual cause of the accident, by 
the increased air pressure it produces in the lung; so 
while usually preceding pneumothorax it will certainly 
continue after it, except in cases of sudden death. 
G 



82 DIFFERENTIAL DIAGNOSIS chap. 

2. Pain in the side. — Must be present by postulate 4. It is 

usually sufficient to attract attention, but may be so slight 
or so mixed up with other discomfort as only to be found 
by leading questions. 

3. Shortness of breath (vide under Quasi- Accidental). 

The Quasi- Accide?ital or Variable Symptoms are really only one, 
viz. shortness of breath or dyspnoea (the quickened 
pulse, the collapse, the sweating, etc., are merely variable 
concomitants of the amount of asphyxia). This short- 
ness of breath may be so slight as to be quite unnoticed, or 
may be so severe as to lead to death, appalling in its 
suddenness, with every conceivable degree between the 
two. For the primary explanation of the degree we must 
draw a distinction between the symptoms setting in 
immediately with the accident, and those which develop 
in the course of a little time. For that which comes on 
at once, one quite sufficient explanation is obvious, viz. 
the share in aeration of the blood previously taken 
by that portion of the lung now collapsed and useless. 
That which arises in continuance of the primary trouble 
may own this same explanation, but probably in associa- 
tion with another, viz. the possible valve-like action of 
the torn pleura allowing an inspiratory pumping-in of air 
to the sac, but preventing expiratory escape, so that more 
and more healthy lung is allowed or forced to collapse ; 
this may go on to a degree incompatible with life, or by 
the establishment of pressure and tension equilibrium it 
may remain stationary, life being still possible. In all 
cases and under all circumstances the ultimate degree of 
shortness of breath has then the above foundation, viz. 
the previous utility of t/ie collapsed area. 

The physical signs of pneumothorax, per se and apart from the 
disease causing it, may be naturally divided into (a) those found over 
the area of separation ; (b) those observed elsewhere. 

(a) The former will be : — 

On inspection. — Nil, unless a large area of lung be collapsed, 
when that side of the chest may be a lktle sunken, and 
probably deficient in movement. 



iv DISEASES OF THORACIC ORGANS 83 

On palpation. — Nil, unless the opening into the sac be a free 
one, when increase of tactile vocal fremitus may be 
appreciated, owing to the freer conduction of aerial 
vibrations with a resonating chamber. 

On percussion. — Hyper-resonance, owing to the air coming into 
immediate contact with the chest wall, and so allowing 
unusual vibratory opportunities. 

On auscultation. — The signs will vary from tubular breathing 
with amphoric resonance — if the opening be patent — to 
complete silence when the lung is collapsed, and the 
opening a mere slit, so that the air pressure in the pleura 
prevents the lung from expanding. 

(b) The latter refer to (1) the increased work thrown on the 
still functionating area of lung, leading to increased loudness of the 
breath sounds previously heard, of whatever nature; (2) the dis- 
placement of the heart's apex beat, which may be much or little, 
right or left, according to the amount and side of the collapsed 
area of lung; (3) frequency of pulse and severity of asphyxial 
symptoms, dependent as before on the previous utility of the portion 
of lung now hors de combat, and possibly in some degree on the 
cardiac dislocation. 

The sequelce and subsequent history of a case of pneumothorax 
depend upon the admission to a living serous membrane of foreign 
material. If this is merely aseptic air, and the opening is such as 
can readily be healed, recovery is likely to be complete with the 
restoration of the status quo ante. If it be tubercular or septic, it is 
almost inevitable that pleurisy of a corresponding type shall arise, 
with its appropriate symptoms. 

With this analysis, the diagnosis of pneumothorax can hardly 
require further discussion, bearing in mind that it always occurs 
suddenly as an acute episode in health or chronic disease. It is, 
however, somewhat frequently assumed that the condition may be 
mistaken for a pathological cavity in the lung. When, as is 
frequently the case, the two coexist, diagnosis is difficult, I admit, 
and probably immaterial ; but under other circumstances the two 
offer more contrasts than likenesses, as may be seen by comparing 
the above with the following : — 



84 DIFFERENTIAL DIAGNOSIS 



INDICATIONS OF A PULMONARY VOMICA 

On inspection. Sinking in of chest from the old fibroid disease 

which remains from the original trouble that 
caused the excavation. 

On palpation. Increased T.V.F. from the consolidation sur- 

rounding the cavity, and from the resonance 
of the chamber. 

On percussion. Dulness and increased resistance, again arising 

from induration and consolidation around the 
cavity. 

On auscultation. Tubular breathing with amphoric resonance, 

frequently adventitious sounds of the nature 
of rales, and clicky or resonating crepitations ; 
the former arising in and from the cavity, the 
latter from the fluid in it and from the consoli- 
dating catarrhal mischief going on around it, 
so that their absence is a good sign as indicat- 
ing inactivity of disease or its obsolescence. 

These are the signs usually ascribed to a vomica in the lung, 
and the reasoning is sound as far as it goes, because chronic 
phthisical processes (tubercular or non - tubercular, vide below, 
Fibroid Phthisis) are far and away the commonest causes of these 
excavations. But even with this causation there are two or three 
conditions that must be fulfilled before the signs will be present in 
typical form : ( i ) it must be fairly superficial to prevent its appro- 
priate signs and sounds being overwhelmed by those of overlying 
healthy or diseased lung ; (2) it must be of fair size, at least as large 
as, say, a nut, to cause amphoric echo ; and (3) it must communicate 
by a patent opening with a bronchus to allow access of air. The 
two acute processes, viz. abscess and gangrene, which may produce 
rapid excavation of the lung, are by their very acuteness sufficiently 
distinguished, qua excavation, from tubercular mischief. 

N.B. — It is advisable, or even imperative, in doubtful cases of 
excavation, to listen to the chest actually while the patient is coughing, 
as well as to note alterations in signs after a cough, because the 
tube or tubes leading to the cavity may be blocked with material 
only to be removed by coughing. 

PHTHISIS 

" An assemblage and progression of symptoms associated with 
and dependent upon the ulcerative, or suppurative, destruction of a 



iv DISEASES OF THORACIC ORGANS 85 

more or less circumscribed non-malignant deposit in the lungs," 
was the late Sir Andrew Clark's definition of the disease, and I do 
not think a better one could be devised, although it excludes 
miliary tuberculosis, for it is wide enough to embrace all the non- 
tubercular chronic destructions of the lung which are associated 
anatomically with suppuration and ulceration. Both before and 
since the enunciation of this definition an enormous amount of 
literature has appeared containing exhaustively detailed descrip- 
tions of the anatomical results of phthisis in the lung, and 
classifications of the disease of such endless variety, that the 
student of the subject must get confused in trying to get an 
intelligent idea of the whole of it ; for under such a weight of 
exposition he is in great danger of losing sight of that unity of 
principle with diversity of result which underlies and explains the 
varying aspects of phthisis and chronic diseases of the lungs. It 
is to this unity of principle that I wish to draw special attention, 
with a few brief notes on the results and conclusions. 

The frequency of tubercular — as compared with all other forms 
of — chronic irritation and destruction of the lung, and the special 
anatomical results of this special form, have led to a tendency to 
view inflammation in the lung as always something special, with 
special laws of its own. Such a view is erroneous and misleading, 
and the first great principle in our present subject is that the lungs 
offer no exception to the rules that govern the processes of so- 
called inflammation, as it occurs amongst vascular tissues anywhere 
in the body. These processes we must briefly indicate in a series 
of paragraphs : — 

1. The collective phenomena known by the name of inflamma- 
tion are the invariable result of a locally acting (not necessarily 
locally produced) irritant of any kind whatever, provided this be not 
sufficiently severe to kill the tissues outright ; and then, be it 
remembered, the processes go on in the surrounding living tissue, 
the dead mass sharing in, or being the efficient cause of, the 
irritation. 

2. The first phenomenon is interference with the freedom of 
circulation through the part, a coincident out-soaking of fluid, and 
the appearance in the area of numbers of small round cells. The 
majority of these cells are of feeble vitality, if not actually dead, 
representing as they do to a large extent the dead and wounded in 
the fight between invaders and defenders. The tissues, too, in and 
near which the fight is going on, suffer in vitality from the disturb- 
ance in their normal circulatory refreshment ; this is the functio 



86 DIFFERENTIAL DIAGNOSIS chap. 

Icesa of inflammation, whether in mesoblastic or epiblastic ele- 
ments. 

3. Paragraph 2 represents the destructive phase of inflamma- 
tion. It may reach any degree of intensity, from the microscopic-in- 
quantity-but-identical-in-quality of the healing of an aseptic wound 
up to the quarts of pus and sloughing of septic cellulitis ; and it 
continues in the immediate neighbourhood of the irritant so long 
as this — or its products — remains in such a condition and position 
as to come in contact with irritable tissues. 

4. Following this, as the defenders locally or generally get the 
upper hand, comes the reparative phase in which granulation tissue 
is formed, consisting of new nucleated cells (the precise origin of 
these and of pus, though perhaps important, has no bearing on our 
present purpose), endowed with vitality because of, and in propor- 
tion to, their proximity to supplies of nutriment in the shape of 
newly-formed blood capillaries and intercellular lymph spaces. 

5. Following granulation tissue comes the formation of fibrous 
or scar tissue, which possesses primarily some peculiar properties : 
(a) it is practically non- irritable, hence should the irritant still 
remain active in situ, it serves to shut it off from its field of opera- 
tion on irritable tissues, and eventually causes its death by isola- 
tion ; (b) though poor in vitality itself, it is not irritating to healthy 
tissues, and has no tendency like dead material to cause a spread 
of inflammation ; (<r) it is extensile and contractile, almost mechanic- 
ally so, so to speak, very different in these qualities from naturally 
existing fibrous tissue, exhibiting either quality to an extreme degree, 
unbalanced by intermingled muscular fibres ; (d) though in general 
it is produced in an amount which is simply reparative, it is' occa- 
sionally liable to excessive growth, as is seen in false keloid and in 
some thickened pleura. 

6. The dead material that arises as the result of the destructive 
phases of inflammation, if left in situ and isolated by scar formation, 
and if it does not become the seat of a fresh development of 
irritating energy (septic microbes, etc.), has a tendency to dry up 
and be converted into cheesy material, and ultimately into a cal- 
careous mass by the deposition of lime salts. 

7. The two phases of inflammation — the destructive and the 
constructive — must go on so long as the irritant remains in contact 
with irritable tissues. The fight must always be to the death or 
impotency of the tissues, or of the irritant. Hence in the case of 
a living and propagating irritant (microbes) it may be prolonged 
indefinitely ; the microbes striving, and, alas ! too often with over- 



iv DISEASES OF THORACIC ORGANS 87 

whelming success, to cause destruction, the tissues as continuously, 
but with indifferent success, to efface their enemies by scar 
formation. 

8. From a given primary focus inflammation may spread by (a) 
direct continuity as the irritant extends its area of influence wider 
and wider (this method of extension, if of any distinct degree, is 
almost conclusive proof of microbic invasion, for a simple mechani- 
cal irritant cannot spread ; a non-reproductive chemical one would 
rapidly become neutralised by combination ; and it is only by direct 
multiplication of the microbe, or by the continued production of 
toxins, toxicogenic zymins, etc., that we can understand the widening 
area of irritation) ; (b) mechanical transference of the irritant to 
other points, either by the blood stream or per lymphatic channels, 
or, especially in the lungs, by air currents or mere mechanical 
dropping under the influence of gravity into parts which are for 
the time being lower than the original focus. 

These are the essential principles of inflammation wherever 
occurring, undeviating in their action, only modified, not obscured 
or fundamentally altered, by the nature of the invading irritant and 
the elementary anatomical details of the organ attacked. 

Of the modifications introduced by the nature of the irritant, we 
must note that in tubercle (the same is true to a certain extent of 
the other infective granulomata) there is a special tendency to the 
early and rapid formation of a small mass or nodule of granulations 
with a vitality and cohesion somewhat in excess of that met with in 
the results of the inoculation of more virulent microbes. These 
nodules would apparently seem to belong to the reparative side of 
inflammation, for they do occasionally — it is true very rarely — 
become quite fibrous even in a miliary tubercle, but owing to their 
low degree of vitality and lack of capillary nutrition they cannot 
individually grow to any size without caseating or softening down. 
Owing to the great pertinacity and multiplication of the irritant they 
are, however, persistently produced in the immediate vicinity of the 
original focus, and by their union and coalescence may constitute 
masses of caseous material as large as the thumb or larger. If the 
irritant be of a more virulent type, the destructive phases of inflam- 
mation are more prominent, with suppuration and tissue death 
(microscopic = necrosis, macroscopic = gangrene), and, possibly, the 
development of foul smelling gases as the predominating processes. 
If different irritants of different virulencies be at work at the same 
or successive times, the results are likely to vary according to the 
above sketch, first one and then another becoming the predominat- 



88 DIFFERENTIAL DIAGNOSIS chap. 

ing feature of the case, e.g. catarrh followed by tubercle, pneumonia 
by gangrene. 

Of the modifications introduced by the anatomical peculiarities of 
the lung, we have only to note the air passages with their enormous 
area of mucous membrane, lined with epithelium, to which air must 
necessarily be freely admitted ; air, too, which cannot always be 
filtered through nasal vibrissas, and which consequently often, or even 
usually, contains multitudes of microbic, mechanical, and chemical 
irritants of every kind. Hence we have (i) an extraordinarily ex- 
tended frontier offering opportunities of invasion; (2) the most 
favourable opportunities for the accumulation, in tubes through 
which air currents are feeble, of mucus and dead epithelial, 
and other cells (catarrhal products), on which microbes may implant 
themselves without opposition, and grow and multiply till they reach 
irritable tissues ; (3) the physical signs of such tubercular nodules 
or of catarrhal and pneumonic products will naturally be essentially 
identical in local details over small areas, for they all produce con- 
solidation or collapse of lung tissue, or sticky fluid contents for the 
air tubes ; it is this which causes so many difficulties in diagnosis. 

We may now apply these principles and their modifications to 
explain the correlated pathology of, and the adjectives applied to, the 
varieties of phthisis. 

Pneumonic Phthisis 

This term may be used to refer either to the amount of con- 
solidation of the lung, or to the clinical history of the case, resem- 
bling at some period of its course a pneumonia (croupous or 
catarrhal). In the former case we have the tubercular nodules 
rapidly forming and coalescing (scrofulous or acute pneumonic 
phthisis of authors) until large areas are involved, giving the 
physical signs of a pneumonia, but without the definite limited 
symptoms of that trouble ; the softening of the masses will add 
still further likeness to the resolution stages of ordinary pneumonia. 
For the latter signification of the term, i.e. a clinical history re- 
sembling that of a pneumonia, it is a common enough event for the 
tubercular nodule to cause an inflammation of a non-tubercular 
nature to surround the original focus with consolidation (tuberculo- 
pneumonic phthisis of authors), and this may occur at any period 
of the progressive destruction. In both these cases the tubercular 
bacilli are the original irritating invaders. But another common 
sequence is the primary invasion of the pneumococcus (croupous) 
or of less definite microbes (catarrhal), causing a wide-spread con- 



iv DISEASES OF THORACIC ORGANS 89 

solidation or pneumonia, and in the weakened tissues and dead 
material thus produced the specific tubercle bacilli find a favour- 
able nidus for growth, and proceed more or less rapidly to con- 
tinue the mischief after the acute symptoms of the original 
invasion have subsided. This sequence of events explains the term 
catarrhal phthisis, though the term might equally well be applied to 
the ordinary cases of not very acute tuberculosis of the lung in 
which large areas are not simultaneously solidified. 

Fibroid Phthisis 

This term includes all varieties of chronic lung destruction, of 
whatever nature, in which the reparative or scarring phases of 
inflammatory reaction have reached a considerable degree and extent. 
Inasmuch as the bacillary or simple irritant invasion is entirely 
a matter of accident, we have the following easily understood 
varieties : — 

Tubercular. Another name or way of expressing a very chronic 
case of tubercular phthisis, in which the fight being a pro- 
longed one, the scarring is very evident. (The term 
must obviously be also applicable to cases of cured 
phthisis.) 
Tuberculo-fibroid. Nearly the equivalent of the first variety, only 
that subsequent to the tubercular scarring other irritants 
continue the inflammatory reaction and healing. 
Fibro-tubercular. In which the primary scarring is due to in- 
definite bacillary or even mechanical (pneumonokoniosis, 
stonemasons' or coalminers', etc., lung) irritants, and on 
the weakened tissues the tubercle bacillus makes a 
descent, and continues the destruction - with - healing 
processes. 
Fibroid. A condition of fibrosis of the lung, starting as above 
(most commonly, perhaps, from an unresolved pneumonia 
or bronchopneumonia), but in the production of which 
the tubercle bacillus never at any time plays any part. 
N.B. — Post-mortem experience would almost lead me to believe 
that in any of these cases the scar may take on a keloid-like exten- 
sion, independent of obvious irritation. 

HEMORRHAGIC PHTHISIS 

When haemorrhage of noticeable extent occurs as the result of 
" ulcerative destruction of the lungs," the blood may either coagu- 



90 DIFFERENTIAL DIAGNOSIS chap. 

late in situ round the focus, or it may also be mechanically carried 
into distant air tubes and alveoli. The ulceration may or may not 
be due to the action of tubercle bacilli ; in the former case, extrava- 
sated blood is likely to be more or less impregnated with the bacilli, 
and in proportion as it is impregnated it acts locally or at a distance, 
like a laboratory plate culture, causing a rapid multiplication of the 
points of infection. (This is the old phthisis ab hajnoptoe. The 
older pathologists did not recognise, as we now do, that the bacilli 
were there before the haemorrhage, and that it is only their exten- 
sion which is due to the bleeding.) In the latter case, when 
tubercle bacilli are not present, the haemorrhage, qua haemorrhage, 
is harmless enough, or, at least, has to be considered from a totally 
different standpoint of causation. 

Miliary Tubercle 

Is a condition in which thousands of tiny nodules are scattered 
through the lungs (and other organs, liver, spleen, etc., including 
tubercular meningitis), and only requires notice here to insist upon 
the fact that it is never a primary form of attack from without of the 
tubercle bacillus. It invariably arises from some caseous or softening 
tubercular * focus within the body, the bacilli being carried thence 
by lymph or blood stream. This focus can always be found by a 
sufficiently close search on the post-mortem table. 

Diagnosis of Pulmonary Tuberculosis 

From the above consideration of the pathology of, and anato- 
mical changes in, chronic and even acute pulmonary disease, it 
will be seen that an accurate and exact diagnosis of their causa 
causans is not to be obtained by physical signs alone. All such 
affections are, or may be, indifferently associated with crepitations, 
rales, and rhonchi, and with consolidation of small or large areas of 
lung, with or without signs of pleuritic involvement. We may be 
inclined in one direction by the localisation of these morbid 
phenomena to an apex or to a base, and led in another by their 
universal distribution over the whole of one or both lungs. The 

1 In all that relates to phthisis the terms ' ' tubercle " and ' ' tubercular " are used in 
strictly concomitant association with assumed specific bacilli. The terms "nodule" and 
' ' nodular " are used in their strict meaning of a little lump, or referring to a little lump. 
It is the confusion in these terms that has led to much confusion in translating the 
meaning of the older authors, who made tubercle the equivalent of a little lump, with- 
out reference to the presence or absence of bacilli, of which, indeed, they naturally 
knew nothing. 



iv DISEASES OF THORACIC ORGANS 91 

family history may show a special proclivity to tubercular disease. 1 
We must weigh the circumstances of occupation as affording oppor- 
tunities for pneumonokoniosis ; we must note with anxiety a failing 
appetite, with wasting and sweating, and carefully watch the pro- 
gress of our patient when acute symptoms (cough, fever, haemo- 
ptysis, etc.) have subsided. But when all these points have been 
duly weighed in the balance, remembering that tubercle may pre- 
cede, accompany, or succeed any other irritant, we shall still have 
before us the one crucial question, "Is the bacillus tuberculosis 
present in the expectoration or not?" Universal consensus of 
opinion warrants the statement that if the bacillus be found, it is at 
any rate a prominent sharer, if not the sole factor, in the production 
of the patient's illness, so that if we would guard against disappoint- 
ment in prognosis and errors in diagnosis, the search for the 
microbe must be undertaken in every case permitting of doubt. 
The most likely cases for error and doubt are the following : — 

(a) Bronchitis and Bronchopneumonia in Babies and Young 
Children. — Here sputum for examination is practically unobtainable, 
and we must rely mainly on the following considerations : — If the 
disease is simple in origin the patient should get well in from two 
to three weeks, and the improvement in the child should correspond 
fairly well to the clearing up of the morbid lung sounds. If the 
child does not rapidly pick up after this time, a very careful search 
must be made for empyema, which very commonly develops and 
retards convalescence. Should no evidence of pleuritic trouble be 
found, and the child still not improve, then tubercle must come 
strongly under suspicion, and every system and part of the body 
must be carefully examined for corroborating or contradicting 
evidence. Pulmonary tubercle under the age of say ten or eleven 
years is practically only of one kind, viz. miliary, or at least very 
widespread, and hence a wide area of persistent morbid phenomena 
will be suggestive. Those other unknown irritants which maintain 
a chronic catarrhal condition have a contrary tendency, viz. one to 
preserve their morbid activity only in one locality, and that usually 
at the base. These basic chronic catarrhs, especially if occurring 
after a specific fever, such as measles, by no means infrequently 
persist, and form the origin of a genuine purely non- tubercular 
fibroid phthisis. 

1 Modern opinion, in more strict accordance with the bacillary or infective theories 
of tubercular processes, is inclined to attribute more weight to the view of direct infec- 
tion by personal contact with a sick relative or friend, or by inhalation of germ- 
infected air of the sick-room, and less to the mere possession of tubercular ancestors. 



92 DIFFERENTIAL DIAGNOSIS chap. 

(b) Repeated attacks of " Cold and Cough" with slight symptoms 
of Mild Bronchitis. — This group of symptoms constitutes the very 
commonest history of the commencement of an ordinary case of 
phthisis, and must, therefore, ab initio, arouse our strongest suspi- 
cions. Sputum may be available, and may decide the diagnosis out 
of hand, but it must be remembered that even tubercle takes a 
little time to soften and ulcerate, so that expectoration may be 
unobtainable, or, again, its examination may yield merely negative 
results. We must then proceed to carefully examine the lungs for 
a small localised area over which the auscultatory phenomena are 
not only pathological, but different from the universally heard 
rhonchus of bronchitis, and suggestive of consolidation. Such are 
commonly, but by no means invariably, found at the apices of the 
chest. They are found frequently enough at the apex of a lobe, or, 
in my experience, often in the neighbourhood of the pericardium. 
I do not think that a visible want of expansion or altered percus- 
sion note is of much use in deciding doubtful cases. By the time 
they are definite enough for observation the general symptoms have 
rendered their aid superfluous. I am accustomed to rely more 
upon the sharpness of the crepitations — "clicky" is the term I usually 
apply to them — and a slight increase in voice and expiratory breath 
sounds. If these go with a pulse frequency, and a loss of weight 
and appetite out of proportion to the apparent illness, I feel at any 
rate judgment must be suspended, and the case declared one of 
doubtful and suspicious nature, and the more suspicious, the 
stronger the lead given by the patient's history, whether family or 
personal. These are the cases that made our predecessors in 
medicine divide their patients up into constitutional types of liabi- 
lity to consumption : the blonde, with thin flaxen hair, the brunette, 
with flushed cheeks, the sprightly or ethereal, the clumsy or scrofu- 
lous ; their descriptions are still true in the main, for they were 
founded on an experience which is still ours. 

(c) Hcemoptysis. — It may be said at once that genuine pulmonary 
haemoptysis, and especially if free or repeated, when found with the 
physical signs and symptoms considered under (h), adds so enor- 
mously to the probabilities of tubercle as to render diagnosis nearly 
certain ; but the symptom is so common and so alarming to our 
patients, that it may be discussed at a little greater length. We 
have already (p. 54) enumerated and briefly mentioned the possible 
causes of haemorrhage, and on p. 152 given the diagnosis between 
haemoptysis and haematemesis. It remains here to consider the 
question commonly enough asked, "What do you expect to hear 



iv DISEASES OF THORACIC ORGANS 93 

in the chest of a patient who comes to you complaining of ' spitting 
of blood ? ' " We may, I think, reply accurately enough by saying, 
" If blood-spitting is his only complaint, it is probable that we shall 
hear nothing." The reasons for this reply are: (1) that in a very 
large proportion of such cases the blood comes from elsewhere than 
the lungs — gums, pharynx, nose, larynx, etc. ; (2) that in again a 
large proportion of the cases in which the blood does really come 
from the lungs, it is symptomatic of advanced heart or lung disease, 
which will have given rise to marked symptoms previous to, and 
different from, the haemorrhage; and (3) it is a common experience 
that we hear nothing — not even the crepitations of blood in the 
bronchioles — in those cases which time shows only too clearly were 
really cases of tubercular haemorrhage. In connection with the 
diagnosis of the causes of pulmonary haemorrhage, I cannot conclude 
better than by quoting a few sentences written by Sir Thomas 
Watson many years ago, and which still hold good. He says 
{Lectures on the Principles and Practice of Physics, 5th edition, 1871): 
" Cceteris paribus, the disposition to pulmonary haemorrhage is in- 
creased by whatever tends to diminish the capacity of the thorax, 
and to compress the lungs, or the heart and great vessels. It is 
partly on this principle that we may account for the frequency of 
haemoptysis in persons with crooked spines: in tailors who sit 
continually in a stooping posture ; in young women who lace their 
stays too tightly ; and even in those who labour under dropsy or 
other cause of distension of the belly." He then quotes in full 
detail a case of vicarious menstrual haemoptysis, and proceeds : "It 
is, however, a melancholy truth that capillary haemorrhage from the 
mucous membrane of the air passages is dependent in a very large 
proportion of cases upon incurable disease — tubercular phthisis or 
organic disease of the heart. When haemoptysis is thus actually 
symptomatic of tubercular disease of the lungs, it is liable to con- 
siderable variety in regard to the period of its first occurrence. 
There are many persons in whom the first attack of haemoptysis 
precedes, even for years, the primary symptoms of unequivocal 
phthisis. There are others in whom the first attack of haemoptysis 
is immediately followed by all the signs which announce the pre- 
sence of tubercles in the lungs." He then mentions heart disease 
and pulmonary apoplexy, and after quoting Andral to say that : 
" Of those individuals whom he had known to spit blood at some 
period or other of their lives, there was only one in five whom he 
did not know to have tubercular phthisis." He deplores his in- 
ability to alter the opinion he had long held and expressed : " That 



94 DIFFERENTIAL DIAGNOSIS chap. 

if from any given number of persons who have been known to spit 
blood — excluding the streaks of bronchitis, the rust -coloured ex- 
pectoration of pneumonia, and injury to the chest — we subtract 
those in whom that symptom was connected with irregularity in the 
uterine functions, and those in whom it was symptomatic of cardiac 
disease, there will be very few indeed left in whose lungs the exist- 
ence . of tubercle or other fatal disease may not be confidently 
predicated." 

Except that we do not now regard pulmonary tuberculosis with 
quite such a hopeless feeling as regards prognosis, these statements 
of Sir Thomas Watson are, I think, as true now as when he wrote 
them. 

(d) Pneumonia that does not dear up rapidly after the Temperature 
has fallen. — Here the very fact that the lungs do not clear up in, 
say, three or four weeks, constitutes in itself proof that something 
other than the pneumococcus is at work. This something may be 
tubercle bacilli or others not yet sufficiently identified (there is just 
a possibility that the lung tissue — the soil — of the individual may 
be peculiarly weak, and allow well known microbes to continue the 
irritation). Expectoration is always present, and can be obtained for 
bacteriological examination, so that diagnosis requires no further 
remark beyond calling attention to the fact that an unresolved 
pjieumonia is not necessarily at any ti??ie tubercular, but may at any time 
become so, and is, therefore, a standing menace to its possessor. 

(e) Chronic Bronchitis. — Vide below, p. 98. Here I can only 
say sputum is again available, and must be examined. 

Of pyrexia in these various cases I have said but little, as its 
indications are of dubious significance. On the one hand, it is 
certain that a slight rise of temperature (101 or less) in the evening 
(especially with early morning sweating) is strongly suggestive of 
tubercle in those cases, as in group (b), where the physical signs 
are doubtful ; but, on the other hand, it is equally certain that 
typical hectic temperature (102, 103, or 104 at night; 97 to 99 in 
the morning) is due more to septic processes, either with or without 
tubercle, than to tubercle itself, so that in the other groups we get 
very little assistance from thermometric observations. 

There is only one other point in phthisis that I propose to 
mention, that is diarrhoea. It is important to remember that it 
may be due to any of the following : — 

(a) Simple dietetic errors, from which phthisis is no protection. 
Inquiry into food will possibly suggest this cause. 

(b) Simple irritability of alimentary tract, which is very common 



iv DISEASES OF THORACIC ORGANS 95 

in these patients, and may be increased by swallowing septic or 
irritating matter which ought to be expectorated. The diagnosis of 
this form can only be made by exclusion, and by noting that it 
moderates or ceases under appropriate treatment, and warning 
against swallowing sputum. 

(c) Tubercular ulceration of gut. The diagnosis will mainly rest 
on the intractability of the diarrhoea, and possibly some tenderness 
of abdomen, together with an exclusive consideration of the other 
three conditions. 

(d) Amyloid or lardaceous disease. This generally admits of 
easy diagnosis from the enlargement of the liver and spleen, and 
considerable quantities of albumen (without pus) in the urine. It 
is very rare for the intestine to be the sole or even the principal 
seat of the deposit. Should this, however, happen to be the case, 
it may be difficult or impossible to differentiate the condition from 
tubercular ulceration. In both cases the patient will probably be 
anaemic and cachectic ; in both the flux will be persistent and in- 
tractable. We may remember that amyloid degeneration never 
occurs in early phthisis before suppuration has been long estab- 
lished ; intestinal ulceration may, on the other hand, be a much 
earlier feature. Diarrhoea from amyloid disease, again, is usually 
stated to be entirely free from abdominal pain, while ulceration is 
frequently associated with colicky disturbances. 

PNEUMONIA 

Of the diagnosis of a well-developed attack but little needs to 
be said. The flushed or bluish face, with sweat standing in large 
drops on the forehead, the working of the alae nasi, the rapid 
breathing, the painful efforts at subduing a distressing cough, makes 
up such a typical picture that we can often diagnose the disease at 
sight ; and when woodeny dulness on percussion and tubular breath- 
ing on auscultation are added, the diagnosis is complete. But there 
are one or two points still that are worth a little discussion, even in 
an elementary work. 

Diagnosis in Early Stages. — Primary or idiopathic pneumonia is 
particularly characterised by the very sudden rise in the temperature 
(probably 103 or 104 within twelve hours), and a corresponding 
sudden onset of symptoms ; while the physical signs, being much 
slower in development, are still in abeyance. These symptoms are 
usually a rigor, or convulsions (convulsions in children often take 
the position of rigors in the adult as an indication of severe invasion 



96 DIFFERENTIAL DIAGNOSIS chap. 

by microbes), speedily followed by headache with intolerance of 
light, frequently enough delirium, and vomiting of a nervous type, 
i.e. independent of food. Now these are precisely the symptoms 
suggestive of an acute toxaemia, or of intracranial inflammation ; 
and hence many cases of incipient pneumonia may hastily be 
assumed to be something more dangerous than ultimately proves 
to be the case. 

Careful attention to the following points may assist us in form- 
ing an opinion, but for twenty-four or even forty-eight hours it is 
often absolutely impossible to make a final diagnosis. 

Inquire of the patient or friends as to any possible local source 
of infection, such as a wound, a boil, or an abscess, or even a blow 
on the head, and especially as to any discharge from an ear ; the 
throat and ears must then be examined for signs of septic mischief, 
and time would not be wasted by asking if the patient has had the 
opportunity of acquiring an infectious disease from a sick friend. 
If negative replies are received to these inquiries, note the pulse- 
respiration-temperature ratio, vide p. 35, which even from the 
commencement is very likely to be markedly deranged in a case 
of pneumonia. Should the indications be still undecided, judgment 
must be withheld temporarily, until a cough with expectoration or 
physical signs come to our aid. 

Central Pneumonia. — It occasionally happens that a pneumonia 
develops in, and remains confined to, the central part of one base, 
and thus the physical signs, even in the later stages, are concealed 
or ill developed. In such cases the sputum becomes a most valu- 
able sign, and quite possibly gives an absolutely decisive indication ; 
it is probably extremely sticky, but little aerated and non-purulent. 
If with these features it is uniformly stained with blood pigment, 
we are justified in saying that some pneumonia is present — the 
staining may be of any degree from rust to prune-juice colour, and 
the deeper it is, the worse the outlook. 

Is Pneumonia a Specific Disease ? — The facts suggesting such a 
theory are : — 

(1) The sudden onset of symptoms before, and independently 
of, the lung consolidation. 

(2) The sudden cessation of the symptoms while the consolida- 
tion still remains. 

(3) The definiteness of the phases through which a typical case 
of the disease passes. 

(4) The undisputed occurrence of small epidemics, and the 
appearance of attacks in which the evidence of infection from a 



iv DISEASES OF THORACIC ORGANS 97 

previous case is overwhelmingly strong (noticed in anxious wives or 
mothers too closely attending their sick charges). 

(5) A microbe of very definite character has been pretty con- 
stantly found in sputum and lungs of typical cases; it has been 
isolated and cultivated, and to a limited extent has been put through 
the tests on p. 26. 

Nos. (1) and (2) undoubtedly prove to a demonstration that the 
symptoms of pneumonia are not due to the lung consolidation as 
such, while (5) offers a plausible explanation of them; and we may, 
I think, sum the matter up by asserting that " One particular 
microbe is capable of producing a form of disease to which the 
term ' idiopathic pneumonia ' is applicable, but that facts do not 
prove that this is the only microbe capable of producing a set 
of clinical phenomena indistinguishable from such pneumonias." 
Accurate post-mortem evidence, coupled with scrupulously exact 
bacteriological work, would, I suppose, clear up every case and prove 
its precise causation, but there can be no disputing the fact that 
consolidations of large areas of the lung, coupled with symptoms 
indistinguishable per se (i.e. apart from the clinical history of the 
case previous to their onset) from those of an ordinary pneumonia, 
do occur in the course of bronchial catarrh, of puerperal, and other 
septic troubles, and of influenza amongst many other diseases. 
Admitting this, it is difficult to believe that the lung mischief is 
necessarily due to diplococcus pneumoniae, and that we must deny 
to other pathogenic organisms — specific or common, known and 
unknown — this power over the lung. Again, on the other side of 
the question, the diplococcus pneumoniae has been found frequently 
in morbid effusions in joints and elsewhere, under circumstances 
strongly suspicious of a causative relation, so that it cannot be said 
to confine its attention to the lungs. 

The only possible deduction from these facts is to give to 
clinical pneumonia a modified specificity, perhaps equal to that 
given to clinical diphtheria (q.v.), while denying to it one so com- 
plete and unequivocal as that given to measles, syphilis, or scarlet 
fever. 



ACUTE BRONCHITIS AND BRONCHOPNEUMONIA 

The late Dr. Sutton used to teach that healthy children did 

not suffer from bronchitis. If this be so, then the zymotics, poor 

feeding, and neglect are responsible for much subsequent disease 

amongst our young population, for bronchitis is a very common 

11 



98 DIFFERENTIAL DIAGNOSIS chap. 

disease in infants, and as bronchopneumonia is a direct extension 
of the morbid processes to the bronchioles and alveoli, it is a 
common difficulty to decide whether a given case shall be called 
bronchitis or bronchopneumonia. My own opinion is that prac- 
tically all cases of bronchitis amongst young children, if severe, have 
some degree of alveolar extension, so that from the point of view of 
treatment the diagnosis is of little moment, being more of academic 
or examinational interest. If dulness on percussion and tubular 
breathing are present over localised areas they settle the matter at 
once, but as these are easily obscured by non-affected lung tissue 
and the rhonchi of the bronchitis, and as children are awkward at, 
or incapable of, deep voluntary respiration, I usually rely upon the 
following two features: (i) The Temperature: if ioi° or over, it 
points to alveolar extension ; if below ioi° and yet above normal, it 
points to uncomplicated bronchitis ; if markedly subnormal, it again 
points to very dangerous and universal bronchiolar involvement. 
(2) Rales and crepitations : if these are so abundant as to markedly 
predominate over the rhonchi of bronchitis, I again assume that 
bronchopneumonia is present. Dr. Osier, in his deservedly popu- 
lar work on medicine, will not allow any difference between 
capillary bronchitis and bronchopneumonia. As regards the nature 
of the morbid process he is obviously right, for one cannot draw 
an imaginary mathematical line between bronchioles and alveoli ; 
but as regards extent in area I think he is wrong, and I would define 
bronchopneumonia as a local (few or many patches), capillary 
bronchitis as a universal, extension of the catarrhal process to fine 
tubes and alveoli. This definition best explains the undoubted 
difference in prognosis ; capillary bronchitis I regard as uniformly 
and inevitably fatal, while recoveries from local consolidation are 
numerous and, indeed, the rule. 



CHRONIC BRONCHITIS AND ITS ASSOCIATIONS 

It is a very common observation that one attack of bronchitis 
(irrespective of the nature of the irritant causing it) predisposes the 
sufferer to another. A little consideration of the pathology of 
inflammation easily explains this. It is almost inevitable that, in a 
mucous membrane that has once been inflamed and shed a good 
deal of epithelium, slight scar changes, diminishing its vital resist- 
ance, should be left behind. Proceeding further, if we allow 
that these changes (scar tissue) will diminish the natural vital 



iv DISEASES OF THORACIC ORGANS 99 

elasticity of the tubes, it is easy to see that with repeated attacks 
two consequences are likely to follow: (1) the stiffening process 
will extend farther and farther down the tubes, or become more 
and more marked in local segments of them ; from this it will 
follow (2) that increased air pressure, whether expiratory or in- 
spiratory matters not, must be felt more and more by the smaller 
air tubes and alveoli, which were never meant to stand such a strain, 
and consequently yield to it, giving us bronchiectasis, local or 
general, and emphysema. If the lung trouble is of such a nature 
as to be associated with much scar tissue, then this may by con- 
traction constrict air tubes, leading to dilation above the obstruction, 
or if it has a distant point of support its contraction may lead to a 
pulling open of tubes. We must not forget, too, that in elderly 
people, at all events, there is yet a third factor, and an important 
one, in the production of these degenerative or fibrotic processes ; 
this is arterial degeneration or wearing out of arterioles, with conse- 
quent imperfect nutritional changes in fine tissues. It is a clinical 
fact that an enormous numerical preponderance of cases of " bron- 
chitis and emphysema " in persons over forty, say, have atheroma 
of arteries well marked, and I believe the association is causative, 
and not an accidental accompaniment of age. We are thus led 
by simple deductive reasoning to appreciate the pathology and 
occurrence of — 



The Pulmonary Complications of Chronic Bronchitis 

(1) Bronchiectasis, of which the principal diagnostic features 
are : large quantities of expectoration, often brought up in 
mouthfuls at a time, and frequently foetid ; this fcetor is a 
most important diagnostic point between bronchiectasis and 
a phthisical cavity, for the latter never or hardly ever possesses 
foetid contents ; otherwise the physical signs of the two 
conditions are almost identical. 

(2) Emphysema, of which hyper-resonance or too great an exten- 
sion of resonance is the main sign, coupled with prolonged 
expiration and shortness of breath out of proportion to the 
cardiac condition or the signs of bronchitis. 

(3) Collapse, arising from constriction of a tube or from plug- 
ging of it by catarrhal products. Over a collapsed area there 
is likely to be a little alteration in the percussion note — 
dulness or woodeny sound — but absence of breath sounds 



3 DIFFERENTIAL DIAGNOSIS chap. 

will be naturally the chief feature, and, possibly, slight fine 
crepitus on very forced inspiration. 

(4) Hcemoptysis, from rupture of a vessel, either owing to de- 
generation or to mechanical stretching, or possibly to venous 
distension in a violent paroxysm of coughing. 

(5) Pleurisy or pleuritic effusion, arising from extension of in- 
flammation or from passive disturbance of circulatory ex- 
changes ; diagnosed by a rub or dull percussion note with 
sgophony, etc. (vide below). 

(6) Bronchopneumonia and capillary bronchitis, arising from ex- 
tension of the catarrhal process to bronchioles and alveoli, 
either in an ordinary and direct manner, or by the insuffla- 
tion of the decomposing contents of a bronchiectasis. 
These are perhaps the most important complications of all, 
for they are very frequently the direct cause of a fatal 
ending to the case. Moreover, tubercular bacilli may suc- 
ceed, by their assistance, in implanting themselves on the 
weakened tissues or catarrhal contents of the tubes. The on- 
set of capillary bronchitis (vide definition above) is marked 
either by a prominent rise (inflammatory reaction), or, more 
probably, by an equally prominent fall, in the temperature to 
subnormal (asphyxial or exhaustive decline). This alteration 
will be associated with a very marked exaggeration of the 
breathlessness and cyanosis, the pulse will speedily become 
extremely frequent, small, and thready, and the patient will 
rapidly pass into a condition of extreme danger from 
asphyxia; in true universal capillary bronchitis he never 
rallies, but cold, clammy perspiration soon appears, and 
death follows in less than forty-eight hours. The diagnosis 
of bronchopneumonia, when associated with a smart febrile 
attack, does not present any difficulty; but when we are 
attending an elderly patient, the subject of chronic bron- 
chitis, we must be on our guard to examine the lungs 
pretty frequently, as this alveolar extension often creeps on 
in a most insidious manner (pleuritic effusion may behave 
similarly, vide below), a little extra cough and shortness of 
breath, a little flushing of the face, perhaps, or sense of 
weakness or exhaustion, being the only outward indications 
of the mischief, which is most serious in its result. If we do, 
however, discover by care such a smouldering danger, we 
must not forget to test the sputum for bacilli, as this is the 



DISEASES OF THORACIC ORGANS 101 

common history of tuberculosis supervening on chronic 
bronchitic trouble. 



PLEURISY AND PLEURITIC EFFUSION 

To discover the mere presence of these troubles is usually easy; 
to estimate aright their clinical significance is far more important 
and difficult. 

Acute Pleurisy 

Symptoms and Physical Signs. — Of the diagnosis of the presence 
of acute pleurisy I shall only say that pyrexia, associated with 
cough and pain in the side made worse by forced respiratory move- 
ments, is very characteristic, and if friction sounds are heard dis- 
tinguishable from pericardial ones {vide p. 126), the diagnosis is 
complete. I have already (on pp. 61 et seq.) drawn attention to 
other more obscure cases of pain in the side. 

Causes of Acute Pleurisy. — These may be divided into the general 
and the local. As regards general causation, experience shows that 
the following are very liable to an attack : — 

(1) Those who are suffering, or are liable to suffer, from rheu- 
matism, acute or subacute. 

(2) Those who are affected with, or recently convalescent from, 
an attack of an acute specific fever, including influenza. 

(3) The victims of chronic nephritis of any form, with its 
associated imperfect elimination of waste products, and its anaemia. 

(4) It is undeniable that a fourth group must be inserted of 
individuals who are apparently in perfect health, but get an attack 
of pleurisy as the result of what is ordinarily termed a chill. 
Recent observations on the subsequent history of such individuals 
tend to reduce the number of genuine idiopathic cases very 
materially, as a large proportion of them have proved to be con- 
cealed tuberculosis. 

The local causes are : — 

(1) Traumatism, blows, fractured ribs, crushes, etc. 

(2) Extension of inflammatory processes — 

(a) From the lung, tubercle, pneumonia, bronchopneumonia, 

infarction, abscess, gangrene, etc. 

(b) From the pericardium (rarely). 



102 DIFFERENTIAL DIAGNOSIS chap. 

(V) From abdominal viscera, liver, spleen, etc., through the 
diaphragm. 
(3) Rupture of morbid collections into the pleura, independ- 
ently of the inflammatory process reaching it — phthisical cavities, 
abscesses, hydatids, etc. 

Pleuritic Effusion 

Symptoms. — Inasmuch as effusion may be, and frequently is, an 
associate or sequel of the acute affection, however arising, the 
symptoms of acute pleurisy will suggest an examination for fluid ; 
but, on the other hand, effusion frequently takes place very in- 
sidiously, without obvious precedent disease or symptoms of suf- 
ficient severity to induce the subject to take medical advice, and 
only a troublesome shortness of breath or vague chest discomfort 
leads him to submit to examination. 

Physical Signs. — On the affected side we find : — 

On inspection. — Some loss of mobility compared with the sound 
side, possibly a visible displaced heart's apex beat. 

On palpation. — Tactile vocal fremitus, absent or much dimin- 
ished, possibly heart's apex beat felt in wrong place. 

On percussion. — Absolute dulness with increased resistance to 
the pleximeter finger. 

On auscultation. — Weak or absent breath sounds, probably of 
a distant tubular character owing to compression of alveoli 
and finer tubes ; a peculiar nasal twang is given to the voice 
sounds, known as asgophony. Heart sounds heard most 
clearly in a displaced position. 

Over the still uncompressed lung the sounds, qua effusion, will 
be healthy, but the breath sounds will be exaggerated from over- 
work. 

Causes of Pleuritic Effusion and Hydro-Thorax: — 

(1) All the causes of acute pleurisy already enumerated, in any 

of which effusion may be a predominant feature, or may 
remain after the acute symptoms have subsided. 

(2) Heart disease, with its obstructed circulation. 

(3) Malignant disease and other growths (e.g. hydatid) within 

the thorax. 

(4) Tuberculosis of lung or pleura, either evident or concealed 

(vide Causes of Acute Pleurisy). 



iv DISEASES OF THORACIC ORGANS 103 

A general review of the above paragraphs leads to an inevitable 
conclusion that pleurisy and pleuritic effusion must in almost all 
cases be reduced to the rank of a symptom, possibly it may some- 
times rise to the dignity of an independent disease, and as a 
symptom it may occasionally possess the importance of causing a 
fatal event ; but, on the whole, its features and pathology must be 
analysed from the point of view of what lies behind, and not as the 
" be all and the end all " of a diagnosis. 

The Nature of the Fluid. — Physical signs alone enable us to say 
that fluid is present, but they give no direct information as to its 
nature — unless, indeed, we have a pointing empyema, which is, or 
should be, very rarely seen nowadays. Indirectly, by their persist- 
ence, they tell us that the fluid is not being absorbed, but this may 
be, and generally is, due to circumstances other than its nature. 
Should there be no indications of these circumstances, such, I 
mean, as obvious morbus cordis or pneumonia, etc., we are then 
justified in saying that this non-disappearance is probably due to 
the fluid not being simple serum, or to there being some hidden 
and persistent cause for it in the thorax, e.g. tubercle or carcinoma; 
cases of simple idiopathic pleuritic effusion resisting absorption for 
any length of time are rare. The symptoms, again, strictly speak- 
ing, are not of much use : excessive sweating, anaemia, weakness, 
and hectic temperature are certainly suggestive of pus, but they do 
not exclude tubercle with simple serous effusion, nor, indeed, car- 
cinoma, which I have found on the post-mortem table after such 
precedent history. There is but one method of ascertaining with 
certainty the nature of the fluid, and that is to withdraw a little by 
a syringe and examine it with the naked eye and (or) microscopi- 
cally. 

The following considerations will show that even now our 
diagnosis is far from complete: the fluid may be (1) clear watery, 
(2) bloody or blood-stained, (3) milky or purulent, (4) stinking. 

(a) If it be clear, it is either hydatid-cyst fluid — which will not 
coagulate on boiling and will show hooklets — or it is serum ; in this 
latter case no strong deduction can be made from the information, 
for every single cause may have at times clear effusion, except 
ruptured abscesses and gangrene, both of which have probably 
given other and clearer proofs of their presence. It is in clear 
effusions that inoculation experiments on animals are so useful in 
clearing up a doubtful tubercular diagnosis. 

(b) If it be turbid or definitely purulent, the suggestion is 
that the attack is strong or the defence weak, which is not very 



io 4 DIFFERENTIAL DIAGNOSIS chap. 

conclusive information ; empyema is common in children and in 
old people without further obvious cause, and also in renal cases 
and drunkards, but I have met with it as the product of carcinoma. 

(c) Blood or blood-stained serum is naturally to be expected in 
severe traumatism or ruptured aneurysm, in purpuric or scorbutic 
patients, but when occurring without such immediately obvious 
antecedent, it certainly leads us strongly in the direction of 
tubercle or carcinoma, for it is very rare in simple or rheumatic 
cases. 

(d) If it be stinking, we have conclusive proof that the microbes 
of decomposition have gained access to the fluid, but how, or why, 
they got there, we must learn from other evidence than their pres- 
ence. Some cases of stinking empyemata unquestionably do 
perfectly well after simple drainage, proving that the access of the 
microbes was not gained by gross lesions. 

It will thus be seen that the nature of the fluid per se gives but 
little definite or decisive indication x as to the real meaning of 
pleuritic trouble ; serum clear or blood-stained, pus, or stinking 
fluid may each apparently occur or succeed one another in the 
same case ; the point is of great importance for prognosis and treat- 
ment, but we must look elsewhere for clearer indications of causa- 
tion. The presence of acute rheumatism, or the history of its 
previous occurrence, an account of severe exposure to weather, a 
present or recent attack of an acute specific fever, of pneumonia, of 
bronchitis or bronchopneumonia, advanced tubercular changes in 
a lung, are all fairly obvious on slight inquiry or observation. So, 
too, heart disease or chronic nephritis will yield unmistakable 
evidence of their presence, if we only bear them in mind as possible 
causes and look for them. Any of these would be admitted as a 
satisfactory and final explanation of the origin of the trouble, beyond 
the natural history and clinical significance of which we need not 
go either for diagnosis or prognosis ; but if the case offers no such 
leading indications, we have now to decide between (i) an unusual 
case of apparently idiopathic pleural effusion ; (2) malignant growth ; 
(3) tubercle of lung or pleura concealed by the fluid. If the fluid 
has persisted, without signs of absorption, for longer than, say, two 
or three weeks without a causative diagnosis becoming reasonably 
certain, we should, I think, empty the chest as completely as possible 
by mechanical means, even in the absence of urgent symptoms or 
other reasons, solely for the purpose of establishing, as far as 

1 Microscopic or bacteriological examination may possibly in some cases give 
absolutely conclusive proof of tubercular or malignant disease. 



iv DISEASES OF THORACIC ORGANS 105 

possible, a fundamental diagnosis from the nature of the fluid, and 
from the changes in the chest produced by its withdrawal. The 
nature of the fluid we have already seen to be very dubious in its 
indications, though something may be guessed from it. The 
changes in the physical signs may be thus analysed : — In simple 
idiopathic pleurisy aspiration will certainly cause a restoration of 
some degree of resonance to the previously dull area, and the lung 
will soon expand with a return of distinct breath sounds, probably 
intermingled with fine and coarse crepitations, owing to the renewal 
of the circulation through previously compressed lung tissue. If 
the case is a tubercular one, it is again probable that there will be 
some restoration of more natural physical signs on percussion and 
auscultation, but it will not be so complete as in the former case, 
and there is likely to be some evidence of patchy consolidation, 
and quite possibly friction sounds will be heard. It is, too, more 
probable that the fluid will return, though in either case this may 
happen. In growth of more gross character it is unlikely that the 
removal of the fluid will alter to any marked degree {vide below) 
the physical signs found previously ; there is no re-expansion of lung 
with renewed air entry, rapid return of the fluid is practically certain 
to take place, and suspicion becomes greater the more rapidly this 
return appears without pyrexial phenomena to account for it. 

If the fluid withdrawn be turbid or purulent, this is in itself 
strong, but not absolute proof against malignant growth. The 
most important point to bear in mind with pus is that the fibrinous 
coagula, etc., are apt to prevent expansion of the lung, so that 
greater care must be exercised in pronouncing judgment from the 
absence of this expansion. It is also very rare — I should say un- 
known — that tubercle, otherwise indetectable, should cause a purulent 
effusion as the first sign of its presence. 



INTRATHORACIC TUMOURS 

Those which I propose to discuss here are: (1) malignant 
growths ; (2) aneurysms. Both have their chief features in common, 
viz. irritation and pressure, and to discuss in detail every variety 
of each, and its separate diagnosis, would require a monograph 
to itself. I only propose to give the principles on which such 
differentiation must proceed; this necessitates as a foundation a 
brief sketch of the nature and anatomical relationships of the two 
affections. 



106 DIFFERENTIAL DIAGNOSIS chap. 

Malignant Growths 

Are in nature — 
(i) Primary. (a) Carcinoma. 

(b) A group to which we may loosely apply the 
term " lymphosarcoma." l 
(2) Secondary. Every growth or form of it which can cause meta- 

static deposits, or invade the thorax by simple 
local extension. 

Their anatomical relationships may be thus tabulated : — 

Starting Point. Progress. 

^ Almost invariably at the root of] 1. Into the mediastina, 



the lung, either in the root 1 
itself or glands of posterior 
or upper mediastinum. 



r -> 



(a) Anywhere in the lung tissue. 
{b) Creeping into the medias- 
tina. 



sur- 
rounding and compressing the 
structures there, and forming 
a large solid mass. 

Into the substance of the lung, 
solidifying it. 

Into and over the surface of 
the pleura pericardium, etc. 



I have grouped these together, allowing a growth to proceed in 
any direction, a course which is theoretically true, and may now 
and again be taken by any of them, but clinical experience in the 
post-mortem room shows that : — 

1. Primary carcinomata almost always spread either into the 
lung tissue or on to the pleura, or both ; they practically never 
invade mediastinal tissues alone. 

2. Primary lymphosarcomata practically never invade either lung 
or pleura, but grow steadily in the mediastina, compressing the lung ; 
the pericardium is surrounded, and may be actually invaded on its 
inner surface, causing effusion and cardiac difficulties. 

3. Secondary metastatic deposits from a distance practically 
always form nodules in the lung substance, solidifying and ifivading it 
without compression. 

4. Secondary extensions from mamma or oesophagus, e.g., are 
the especial tumours which may spread in any direction. 

1 This term must include true sarcomata, and also the ill-understood enlarge- 
ments of lymphatic glands, lymphadenoma, Hodgkin's disease, etc. 



DISEASES OF THORACIC ORGANS 



107 



Aneurysms 

May be classified according to the part of the arch from which 
they spring, but I think more usefully according to the clinical indi- 
cations, thus : — 



Anatomically. 

Of the ascending arch. 
Of the descending arch. 
Of the descending thoracic 
aorta. 

Of the transverse arch. 



Clinically. 
The aneurysms of physical signs especi- 
ally : 

(a) Externally bulging tumour with 

expansile pulsation. 

(b) Dulness on percussion. 

(c) Audible bruits. 

The aneurysms of symptoms, principally 
or entirely pressure effects on neigh- 
bouring soft tissues (vide p. 1 08). 



The progress of any aneurysm — upwards, downwards, forwards, 
or backwards — is governed by the precise point in the circumference 
of the vessel at which it first starts, spreading from that point in 
all directions except towards the parent vessel. 

This sketch shows that the two conditions cannot be separated 
by anatomical considerations alone. We will now discuss in parallel 
columns the more likely explanation of certain conditions. 



Sex. 
Occupation. 

Age. 

Alcohol. 
Syphilis. 



Aneurysm. 

Many times commoner in 
males. 

The more laborious oc- 
cupation probably ex- 
plains the greater fre- 
quency in men. 

Usually thirty-five to fifty. 



Excess undoubtedly a pre- 
disposing factor. 

Is undoubtedly also a pre- 
disposing factor. 



Growth. 

No predilection for either 
sex. 

Would seem to have no 
influence in inducing a 
growth primarily. 

Primary commoner under 
thirty-five, but second- 
ary at any age corre- 
sponding to the primary 
growth. 

Without influence. 

Has no influence on or- 
dinary growths ; and 
gummata, large enough 
to cause doubt, are ex- 
cessively rare. 



io8 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



Complaint of 
pain. 



Inspection of 
patient. 



Auscultation. 



Aneurysm. 

Acute pain is certainly 
suggestive in cases of 
doubt, but no conclusive 
evidence from this point. 

Bulging expansile tumour 
pathognomonic ; but, of 
course, usually no evi- 
dence from inspection 
in cases of doubt. (Ede- 
ma of an arm occasion- 
ally seen, but of one 
side of chest alo?ie very 
rarely if ever. 



A systolic or double bruit, 
if not traceable to val- 
vular disease, is very 
suggestive ; even if 
valvular it only loses 
significance if patient 
be young and has suf- 
fered from a recognised 
cause of endocarditis. 
The degenerative pro- 
cesses of age tending 
as much to aneurysm 
as to valve destruction. 



Growth. 

If present it is more 
commonly a dull op- 
pressive pain, but neur- 
algia may occur. 

A mass of enlarged glands 
or growth above clavicle 
also pathognomonic ; a 
malignant tumour else- 
where is very suggestive 
in doubtful cases. 
(Edema of one side the 
chest wall very sus- 
picious, and if without 
oedema of arm almost 
conclusive. 

Bruits have no connection 
with tumour as such ; 
may occasionally occur 
if heart is displaced, 
or aorta or pulmonary 
artery distorted, but 
this is very rare. 



Pressure and Invasion Effects 



On lungs. Usually causes compres- 

sion only, with irritat- 
ing cough, but may 
start an acute inflamma- 
tory attack with free 
haemoptysis. 



May cause compression 
only by growing on the 
pleura {q.v.), but more 
frequently assumes the 
characters of an insidi- 
ous consolidation — 
often multiple in 
secondary infection — 
and only at the last 
when breaking down 
causes aspiration-bron- 
chopneumonia. 



DISEASES OF THORACIC ORGANS 



109 



On trachea and 
bronchi. 



On pleura. 



On veins. 



Growth. 

Probably causes only a 
slowly progressive 
shortness of breath from 
compression, which also 
leads to collapse of cor- 
responding area of lung. 

A clear or blood-stained 
effusion, very common 
when the growth reaches 
to and spreads over the 
pleura ; it is probably 
more due to venous 
blockage than a real 
inflammatory reaction. 

Tumour of size or extent 
to be still doubtful fre- 
quently catches the in- 
tercostal veins, causing 
oedema of chest wall ; 
also the vena azygos, 
causing enlargement of 
abdomino - thoracic 
veins; the left innomin- 
ate, too, or even a vena 
cava, may be caught 
early. 

Is now and again blocked 
by a growth, and occa- 
sionally chylous ascites 
has appeared from this 
cause. 

Tumours of thorax proper 
more rarely than aneur- 
ysm cause dysphagia ; 
should they do so its 
amount is likely to be 
unvarying. Carcinoma 
of the oesophagus itself 
is the only likely one, 
and then the gradual 
but persistent history of 

1 A peculiar shock synchronous with the pulsation of the aneurysm, felt by two 
fingers laid on the trachea when extended to its utmost by throwing back the head 
as far as possible. 



Aneurysm. 
Tracheal tugging l very 
characteristic if present ; 
may cause a bronchitis, 
and possibly dyspnoea, 
but vide Nerves. 

Acute pleurisy a much 
commoner result than 
quiet effusion ; this is 
because an aneurysm is 
much more acutely ir- 
ritating than a solid 
neoplasm. 

Aneurysm, until too large 
to be mistaken, rarely 
presses on any vein ex- 
cept the left innominate, 
and hence the oedema 
mentioned under In- 
spection not usually 
available in doubtful 



Thoracic duct. Practically never inter- 
fered with by a doubtful 
aneurysm. 



On oesophagus. 



Aneurysms cause dys- 
phagia, but when it 
arises from this cause 
it is likely to vary in 
degree on occasions. 



DIFFERENTIAL DIAGNOSIS 



On nerves. 



On bones. 



Effect of rest 
or treatment. 



Duration of 
symptoms. 



Aneurysm. 



The intermittent beating 
of an aneurysm appears 
to be more irritating 
than a growth ; the re- 
current laryngeal is the 
nerve par excellence 
of aneurysmal trouble, 
being frequently paral- 
ysed by small aneurysms 
of the arch. 

Destruction of bone by 
aneurysm is very pain- 
ful. 



The symptoms of aneur- 
ysm show spontaneous 
variations in intensity 
which it is difficult to 
account for ; they are 
almost invariably im- 
proved, for a little while 
at all events, by rest 
in bed and other treat- 
ment. 

From clinical histories it 
would appear certain 
that aneurysms may 
last for a long time 
before causing a fatal 
event, hence a history 
of symptoms for many 
months or a year or 
two is very suggestive 
of aneurysm as against 
growth, though perhaps 
more against either of 
them. 



Growth, 
dysphagia as the only 
symptom is the 
strongest circumstantial 
evidence. 
A growth appears to cause 
but little active irrita- 
tion to nerves, but no 
general rule can be laid 
down. Pain is certainly 
less common in growth 
than in aneurysm. 



Intrathoracic growths 
rarely reach and erode 
bones, but one growing 
from the bones of the 
thorax would cause pain 
not so acute as that of 
aneurysm. 

The symptoms of growth 
rarely show even the 
faintest trace of im- 
provement under rest 
and treatment, while 
judgment is suspended. 



All cases of definite tum- 
our end fatally within a 
year, hence if condition 
has early and rapidly 
become severe, it is so 
far in favour of growth 
v. aneurysm. 



iv DISEASES OF THORACIC ORGANS in 

These points, I think, include the bulk of the evidence we shall 
have to weigh in a given case. Few only of them are decisive or 
pathognomonic, but if all are carefully considered I think we shall 
usually arrive at a correct conclusion. 



CHAPTER IV— Continued 

DISEASES OF THORACIC ORGANS 

Section II. — Diseases of the Heart and Pericardium 

Errors of judgment — if not of actual diagnosis — occur more 
frequently in connection with heart disease than with the troubles 
of any other organ. The reason is somewhat as follows : — Before 
the days of the invention and perfection of the stethoscope heart 
disease was either not diagnosed at all, or it was guessed at by pain 
and morbid sensations in the thoracic cardiac area, or it was 
recognised by evidences of circulatory disturbance and the character 
of the pulse. These indications, without the assistance afforded 
by the stethoscope, were apt to be misleading. Now the pendulum 
has swung too far the other way, and, armed with an instrument of 
precision, we are all too apt to think we can immediately diagnose 
heart disease by bruits thus brought within the sphere of our 
objective consciousness. This is just as great a mistake as the 
former condition of uncertainty. That we can thus detect a 
leaking valve or a stenosed orifice must in general be admitted — 
though even here great caution is necessary in interpreting our 
aural perceptions — but this is often enough a very different matter 
from morbus cordis. Sir Andrew Clark was, I believe, the first to 
draw public attention to this. He compiled a very long list of 
patients in whom he had by systematic examination detected a 
cardiac murmur, but whose symptoms and complaints, as he 
showed, had no derivation whatever from a diseased heart. His 
experience we all of us can now confirm from out-patient practice, 
but it seems somehow to have escaped the recognition it deserves 
at the hands of students and practitioners. 

It may then well be asked what are the features (symptoms 



chap, iv ISEASES OF THORACIC ORGANS 113 

and physical signs in combination) by which we are to recognise 
genuine heart disease. The conditions leading to a suspicion of 
heart disease are divisible into two main groups: (1) local in the 
thorax or cardiac area; (2) general, expressed in or by distant 
organs or tissues ; and each may again be divided somewhat 
indefinitely into symptoms and physical signs (p. 21). We will 
proceed to comment briefly on each division. 

Local Thoracic Symptoms which may Indicate the Presence 
of Morbus Cordis 

1. Pain. — Pain is a very variable feature indeed. It may be 
slight, or it may be extraordinarily severe (typical angina), and 
almost any degree of it may be associated with a cardiac condition 
of absolutely no moment at all, or of one of the very greatest 
danger to life. The only general statement that can be made 
about it is, that when due to the more serious troubles, it is very 
liable to spread from its original position and extend to the right, 
or to the upper chest and down the left arm. On the other 
hand, when owning a gastric (its most common source) or other 
than cardiac origin, it more commonly remains fixed to the cardiac 
area. It must not be forgotten that the pain of aneurysm, of 
pericarditis, and of left pleurisy, all instances of serious organic 
disease, more commonly also remain as a stationary pain. In any 
and all cases we must, however, make a careful physical examina- 
tion, for by the results of this our judgment of the pain is, after all, 
mainly influenced. Pain alone must not be accepted as evidence 
of morbus cordis, though, when we are satisfied that the pain is 
genuinely severe, we must be doubly cautious in exonerating the 
heart, even if at the time of examination there remains very little 
or no evidence of abnormality. 

2. Shortness of Breath may be very briefly dismissed, inasmuch 
as it may be due either to pulmonary or cardiac conditions, and it 
is only a physical examination of the patient that can determine 
which. From either source it is probably associated with cough, 
and made worse by physical exertion. That produced by cardiac 
disease is perhaps more definitely relieved by raising the patient to 
a sitting posture. 

3. Cough. — Cough perhaps more properly belongs to the general 
group of back pressure symptoms, but as its alternative causation 
is local, it may be mentioned here. If due to cardiac disease, it 
will be either dry, ineffectual, and useless cough, and is then 

1 



ii4 DIFFERENTIAL DIAGNOSIS chap. 

suggestive of nervous irritation, perhaps aneurysm, or it will be 
accompanied by some expectoration, but this will be simple frothy 
mucus, unless, indeed, there be hemorrhage, when the mucus will 
be blood-stained or replaced by pure blood {vide Haemoptysis, p. 
54). If pus or other organic elements be present, it is a certain 
demonstration that the cough is not purely cardiac in origin. 

4. Palpitation. — This simply means that the beat of the heart 
has become perceptible to the owner of the organ. It is extremely 
common in all sorts of diseases and conditions of ill-health, and 
especially as the result of mere introspection and morbid self- 
consciousness. Accordingly, when standing alone, without objective 
signs of morbus cordis, it is almost an indication against that con- 
dition as its real source ; but when associated with definite abnor- 
malities of mechanism or rhythm, and especially if then constant, 
it acquires considerable significance in the case. 

We thus see that the local symptoms, without exception, 
require a careful physical examination to determine their value 
and significance. 

Local Thoracic Physical Signs which may indicate the 
Presence of Morbus Cordis 

These include everything which can be seen on inspection, felt 
by palpation, appreciated by percussion, or heard on auscultation. 
I do not propose to discuss these in any detail, but shall merely 
indicate seriatim what aids they give us in diagnosis. 

Inspection is very frequently quite negative in its results. It 
may show a heaving impulse of great hypertrophy, or the pulsating 
tumour of an aneurysm ; the apex beat, too, may be visible to the 
eye, and its position is of great importance {vide p. 102 for its use 
in pulmonary diseases). A rippling wave of apex beat is suggestive 
of irregular action, or possibly of pericardial effusion, and recession 
near it in systole might possibly indicate adherent pericardium. 

Palpation will further determine the apex beat and be convincing 
of a strong, heaving beat. It may rouse suspicion of irregular heart 
action. Stress is laid by some on a thrill which may possibly thus 
be felt. It certainly is corroboration of probable mitral stenosis 
when a doubtful presystolic bruit is heard, but is frequently felt 
with failing heart from any lesion, and also may be appreciated 
often in thin subjects whose hearts are above suspicion, so that I 
hold it very cheaply unless other and more certain indications of 
trouble are present. 



iv DISEASES OF THORACIC ORGANS 115 

Percussion gives, with very variable results, the area of uncovered 
heart, and possibly some idea of the gross size of the organ. But 
it is so subject to personal variations in the observer, so liable to 
vary in health in different individuals, so subject to fallacies from 
the position of the lungs in health and disease, that it is wise to 
reduce it to a very low level of diagnostic utility. The preposterous 
claims made on its behalf by the recent upholders of the Schott 
(and other) systems of treatment have reduced its value still lower, 
and left it as an object of ridicule to thoughtful men, at any rate as 
indicating the size of the heart. It is, however, of some little use 
in helping us to differentiate between a pericardial effusion and a 
hypertrophied heart. 

Auscultation. — By auscultation we become aware of several 
factors in the heart beat which are of very unequal significance 
individually, but collectively constitute our most important know- 
ledge of the condition of the heart. They may be enumerated as 
(1) the ordinary sounds of the heart; (2) the frequency of the 
beat; (3) the regularity of cardiac action and its rhythm; (4) ab- 
normal sounds or bruits added to or replacing the natural sounds. 

(1 and 2) The Ordinary Sounds and Frequency. — In health it is 
well known that the first sound should be materially longer than the 
second, the now classical lubb-dup well representing the difference. 
As the frequency of the rate increases this difference must, of 
course, absolutely diminish, and in rates of over (say) 150 is practi- 
cally inappreciable ; but when moderate or low frequency is present, 
even in the absence of other abnormality, a comparative shortening 
of the first sound is a serious indication of some change in the 
action. It may indicate mere nervous hypersensitiveness, and 
then the rate is likely to be high, and other evidence of nervous 
instability may be present in the patient. More usually, and 
especially with moderate frequency of beat, it is suggestive of 
muscular debility or hurry, probably the result of degeneration, or, 
at least, of imperfect nutrition, and makes us anxious about the 
supervention, already present or to come, of a pathological yielding 
of the muscle and incapacity to continue to stand the strain of 
present pressure. 

(3) Regularity. — So long as the action of the heart is regular, 
and its rhythm even, so long may we make a very substantial 
deduction from the prognostic gravity of almost any evidence of 
defective mechanism or circulatory disturbance. If irregularity be 
detected especial care must be taken to ascertain if it be a regular 
periodic irregularity, i.e. an occasional dropped beat say every four, 



n6 DIFFERENTIAL DIAGNOSIS chap. 

five, or six beats, or if it be a totally irregular irregularity, defying 
exact description, and rhythm totally absent. The former is often 
a harmless condition, and may even be beneficial to a heart 
working under some unusual strain, so that in the absence of other 
definite indications of cardiac failure it requires only to be noted 
for future reference, but is not to be treated by direct efforts at 
cardiac medication. The latter, a tumultuous irregularity with 
many beats of very variable strength, is a very grave sign, and 
indicates the urgent need of prompt interference on behalf of an 
overburdened heart. 

(4) Abnormal Sounds. — The presence of an endocardial bruit 
{vide p. 127, to differentiate endo- from exocardial bruits) heard in 
the situation and conducted in the direction usually laid down in 
text-books, is strong evidence of leakage through, or narrowing of, a 
valvular orifice, but the deductions as to cardiac disease to be made 
from this evidence are of very unequal importance in different cases. 
In rheumatic fever or other disease, such as the specific fevers, 
known to be a possible cause of endocarditis, the first occurrence of 
a bruit is of very great importance, for we then know that a valve 
is inflamed and softened, and we get a strong indication for giving 
such valve as much rest as possible. Again, in a case of smoulder- 
ing but persistent pyrexia, the source of which is not obvious, if we 
hear a cardiac bruit which was not present before, or even if we 
were previously aware of its presence, but it seems to vary in char- 
acter at times, it will throw strong suspicion on that valve as the 
seat of a septic or simple inflammation, keeping up the temperature 
and threatening very serious danger. Thirdly, when some of the 
features of circulatory disturbance through an organ or district are 
present, a bruit is certainly suggestive of central cardiac failure as a 
probable contributory factor, though regularity and evenness of the 
cardiac beat are much more important features than the bruit itself. 
In the more chronic cases of valvular trouble, where a bruit or bruits 
have been known to exist for some time, neither the bruit nor the 
precise form of trouble indicated by it is of great importance, for 
we can neither treat the one nor place any great reliance on the 
accuracy of the other. Speaking then in general terms, bruits are 
only of value to remind us (1) when they first appear, they are 
evidence of a softened valve which may yield on pressure ; (2) 
when old, that the heart is working with imperfect machinery, 
which has not the same elasticity for emergencies that the original 
sound mechanism possessed. 



DISEASES OF THORACIC ORGANS 117 



General Symptoms in other Organs which may indicate 
Morbus Cordis 

There are at least two factors in the production of those symp- 
toms which are exhibited by other organs or areas, but which are 
usually accepted clinically as indicative of cardiac disease. They 
are : (1) the work of the heart and aorta; (2) the work of the smaller 
arteries, arterioles, and capillaries interacting with the lymphatic 
circulation through the part in question. 

The heart is a driving and suction pump, introduced into the 
closed system of tubes, by means of which the blood is kept circul- 
ating, and as such its nervous, valvular, and muscular mechanisms 
are perfectly adapted for fulfilling its part in the total result, viz. 
that of keeping up a sufficient head of pressure in the aorta and 
pulmonary artery, and relieving by suction the largest venous trunks 
of their low pressure contents. The aorta in turn, distended and 
stretched by this charge of blood at high pressure, should, by its 
elastic recoil, be able to transmit the charge and pressure in gradu- 
ally diminishing degrees to the arteries smaller than itself. The 
greater or less frequency of the heart beat, and its greater or less 
force, are regulated by the central nervous system only according 
to the very general needs and conditions of the body at large as a 
whole. It is to the second of the above factors, viz. arteriolar, 
capillary, and lymphatic action that we have to mainly look for the 
regulation of the blood supply for the local needs of individual 
organs for particular purposes, and also for an explanation of the 
finer problems of local nutrition and function. That this is in 
many cases the most important factor is strongly suggested, if not 
proved, by cases where death has taken place with the patient in a 
water-logged condition, and yet post-mortem examination has shown 
the heart itself healthy enough, in both muscle and valve, to keep 
up its part of the circulation .for a long time if local conditions had 
allowed or assisted their share of work to be done. It must be 
admitted that improvement in the heart's action is frequently fol- 
lowed by the happiest possible results in distant parts, so that it is 
impossible in clinical medicine to separate and identify the exact 
shares of each factor ; none the less the effect of digitalis or supra- 
renal extract on the one hand, and of iodide of potassium, nitro- 
glycerine, or erythrol tetranitrate on the other, compel us to bear 
in mind the peripheral as well as the central circulatory factors. 
Whichever of the two is at fault, or if both be so, the ultimate local 



n8 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



result from a clinical point of view is much the same. It is to be 
remembered, too, that the precise nature of any valvular defect in- 
fluences only the time when circulatory disturbances appear, and 
then the order or sequence in which they occur ; it has no general 
influence on the result, provided that cardiac muscular failure 
actually supervenes. The result itself is, in the first place, a dimin- 
ished arterial supply of fresh blood, together with an imperfect or 
inadequate removal of the impure venous blood, and renewal of 
nutrient lymphatic plasma. This circulatory disturbance leads in its 
turn to interference with the work of organs with an active function, 
and to oedema or effusion in areas of less functional activity. In 
the second place, this sluggish capillary venous and lymphatic 
circulation, with excessive pressure on the venous side, leads to an 
alteration in the quantity and quality of the natural exchanges 
between blood capillaries and lymphatic channels, and, in fact, alters 
in toto the vital conditions existing in the part in question. Thus 
we find not unfrequently that a venule actually ruptures with gross 
effusion of blood, or individual red cells escape and die in an extra 
vascular situation, or finally the blood may coagulate in the venules 
from unnatural composition, leading to a condition known as in- 
farction. Ultimately, but gradually, fibrin coagulates from the altered 
lymph, and causes a thickening of the capillaries and fibrosis of the 
tissues, and the pigment from the dead red corpuscles stains the 
tissues. Again, we have embolism occurring, not as the result of 
general circulatory conditions, but owning a particular cause in 
either loosened vegetations from endocarditis, or clotting of blood 
in the irregularities of a cardiac chamber, with subsequent loosening 
of the clot into the circulation. The symptoms occurring in these 
various ways throughout the body may be tabulated briefly as 
follows : — 



Organs. 



■Lungs. 



Symptoms of back 
pressure. 

Shortness of breath, 
cough dry or with 
simple frothy mu- 
cous expectoration, 
moist sounds at one 
or both bases. In- 
farction or embolus 
leads to bloody 
sputum, and prob- 



Post-mortem appearances 

known as "heart " 

organs. 

Drier than usual and 
tougher, more re- 
sistant to attempted 
laceration by finger; 
probably discoloured 
from old blood pig- 
ment (brown indur- 
ation) ; round or 
wedge-shaped area 



DISEASES OF THORACIC ORGANS 



119 



Organs. 



Symptoms of back 
pressure. 



ably pleuritic pain 
and rub with physi- 
cal signs of con- 
solidation : this used 
to be termed pul- 
monary apoplexy. 

Pleura. Pleural effusion com- 

mon, with appropri- 
ate physical signs. 

Liver. Tender or even pain- 

ful, and somewhat 
enlarged to the ex- 
amining hand. 

Spleen. Possibly enlarged, may 

be vague pain in 
region. 



Stomach and intes- Dyspepsia, flatulence, 
tines. and constipation fre- 

quent ; severe vom- 
iting often seen. 

Kidneys. Diminution in secretion 

even to almost com- 
plete suppression ; 
slight albuminuria 
very common. 

Brain. Headaches, confusion 

of mind, sleepless- 
ness, noises in head, 
flashes of light, 
etc. ; apoplexy of 
some form common 
enough. 

Limbs. Pitting oedema, especi- 

ally in the legs. 
Emboli of arteries. 

It is particularly important to remember that any organ whose 
vitality and circulation are thus interfered with is in a condition in 
which very slight irritation will cause an acute outburst of infiam- 



Post-mortem appearances 

known as " heart" 

organs. 

of consolidation = 
infarction or em- 
bolus. 



Excess of fluid in the 
cavity. 

Congestion of intra- 
lobular veins, well- 
known nutmeg liver. 

Very firm, may be 
small or large, and 
possibly wedge- 
shaped areas of em- 
bolism. 

Veins very prominent, 
and mucous mem- 
brane dark and 
congested ; possibly 
slight ulceration. 

Kidneys very firm on 
section; cortex 
equally congested 
with the medulla. 

(?) serous apoplexy ; 
brain often seems 
more juicy than 
normal. Embolus 
a well-known cause 
of softening. 



120 DIFFERENTIAL DIAGNOSIS chap. 

mation. Bronchitis and acute nephritis are thus two very common 
complications, and it is often a matter of some importance, but 
great difficulty, to determine whether the bronchi and kidneys are 
simply venously congested or actively inflamed. I am accustomed 
to rely upon a muco-purulent v. mucus sputum, and the presence 
or absence of dry musical rhonchi in the one case, of epithelial 
casts with facial oedema in the other case, as the most reliable 
points of distinction. 

Such, then, are the means we have for determining the presence 
of real heart disease, and, like similar evidence on any other point, 
each factor has to be weighed first individually, and then in addi- 
tion to, or subtraction from, all other factors, and a balance struck 
with every possible care. 

The matter will be referred to again in dealing with nervous v. 
valvular and muscular heart troubles (vide pp. 137 et seg.). 

We may now consider the pathology of, and the meaning of, the 
terms — 

HYPERTROPHY AND DILATATION, COMPENSATION 
AND FAILURE 

Hypertrophy 

It is a provision of nature, distinctly tending to the preservation 
of individuals, that healthy muscle should increase in volume and 
strength (growth or hypertrophy) in proportion to the work it is 
called upon to do, provided that this at first lies within the original 
capabilities of the muscle. The heart is no exception to this rule, 
and when its circulatory work from any cause (nervous, valvular, or 
connected with increase in general blood pressure from kidney 
disease) is persistently maintained above its original average, the 
cardiac muscle hypertrophies or grows to meet the demand, pro- 
vided that the nutritional powers in general of the individual are 
fairly good. Temporary increase in work is inherently provided for 
by a reserve excess of potential energy over that habitually put forth. 

It is easy to understand in general terms that if the mechanism 
of the heart was originally adapted to work with the greatest pos- 
sible efficiency (and we have every reason for such belief), any 
alteration in that mechanism must involve increased expenditure of 
energy to produce the same result, i.e. increased work. We have 
just seen in the previous paragraphs that the symptoms of disease 
of the heart as expressed by organs other than itself are largely (the 



iv DISEASES OF THORACIC ORGANS 121 

vasomotor factor must not be forgotten) indicative of failure of the 
heart to do this increased work. All the means which unaided 
nature can take to bring about a fresh balance of work and power 
are collectively spoken of as compensation, and hence compen- 
sation clinically means regained (if lost) or maintained capabi- 
lity of the heart to do its work under unusual or altered conditions. 
For a permanency this is, to all intents and purposes, hypertrophy. 
Temporary natural compensation was mentioned above as a mere 
use of potential inherent energy, and artificially we can produce 
temporary compensation by diminishing the work, as by rest in bed 
or vasodilator drugs. 

Following this argument, it is obvious that hypertrophy has 
only one cause — increased work. It is actually the result of, and 
can only be equal to, this increase, and then it must logically be 
deduced that the symptoms of hypertrophy are — the absence of 
symptoms of heart disease. Disappearance of these symptoms 
when present means the development of compensation, and if per- 
manent this means hypertrophy. 

It must be admitted that there are circumstances under which 
hypertrophy may be indirectly the possible cause of some trouble. 
If, for instance (as in athletes, soldiers, etc.), great physical exer- 
tion has called forth considerable hypertrophy, then, when the work 
is permanently given up, the heart probably will not diminish in 
bulk in proportion to its diminished duties, and its beat may 
become inconveniently apparent to its owner. It is possible that 
its powerful action may rupture an artery that is healthy. Certainly 
it is a source of danger to vessels that are not healthy, and arterial 
disease and degeneration are unfortunately only too frequent 
results of the same conditions as those which require hypertrophy 
of the heart. In this sense hypertrophy of heart may be described 
as a predisposing factor in cerebral haemorrhage, but in all other 
senses hypertrophy is a purely defensive expression of nature — a 
physiological and not a pathological phenomenon. 

Dilatation 

We may say at once that this term is used in two distinct, and 
in some respects almost opposed, senses. The first is a mere 
mechanical increase in the capacity of a chamber. The second 
sense takes note of only one of the possible consequences of this 
increased capacity, and is the equivalent of cardiac failure. 

As regards the first meaning, theoretical considerations would 



122 DIFFERENTIAL DIAGNOSIS chap. 

show that it is an inevitable and universal result of valvular in- 
capacity, though I am strongly inclined to doubt if it is possible to 
prove the position by post-mortem evidence (the conditions of rigor 
mortis, and the effects of pressure upon dead muscle, do not suffi- 
ciently closely correspond to the reaction of living muscle to its environ- 
ment) ; anyhow, the occurrence of dilatation in this sense has no 
possible importance from a clinical point of view, provided that the 
energy of contraction and the strength of the chamber in question are in- 
creased in proportion?- the object of the muscular walls being merely 
to empty the cavity with sufficient force. 

The second sense in which dilatation is used is exactly repre- 
sented by the absence of this requisite energy of contraction and 
absolute strength, and it is precisely this that is the cause of the 
symptoms of morbus cordis. This is heart failure, or absence of 
compensation. It is under these circumstances that a previously 
hypertrophied heart becomes a nuisance to its possessor by its 
tumultuous efforts to cope with the work to which it is no longer 
equal. It is when this failure or stretching becomes excessive that 
relative incompetency of healthy valves supervenes, for they are no 
longer capable of closing an orifice which has become too large. 



DIAGNOSIS OF HYPERTROPHY AND DILATATION 

As the presence of one or other or both of these conditions 
is, one might say, the very essence of 99 per cent of cardiac patho- 
logy, the recognition of them becomes at once the cardinal point in 
diagnosis. 

Of dilatation in its first or simple sense there is no positive objec- 
tive sign at all, and its presence is a matter of no moment if the 
requisite muscle strength is present to compensate it. Its pre- 
sence is assumed in all cases in which a large heart is due to val- 
vular alterations; in other cases {e.g. that due to renal disease — 
so-called concentric hypertrophy) it is probably absent. 

In all cases, and in any sense of the word, the condition of 
dilatation, as well as that of hypertrophy, demands for its presence 
a heart larger than usual (i.e. for an average environment of age, 
work, etc.), and therefore we require as the first element in diag- 
nosis the signs by which we may recognise an enlargement of the 
heart. 

1 It must be remembered that this proportion is a large one, viz. the cube of the 
figure representing increase in diameter. 



DISEASES OF THORACIC ORGANS 



123 



The ordinary physical signs by which this is done, and the 
principal fallacies, are the following : — 

Fallacies. 
These physical signs found by in- 
spection, palpation, and percus- 
sion may be : — 

1. Obscured — as by abundant fat 
or muscle over the chest, by 
emphysematous lung, by peri- 
cardial effusion. 

2. Rendered unduly prominent by 
wasting of fat or muscle, by re- 
traction of lung, by deformity 
(pigeon breast, Pott's curvature, 
etc.) of the chest. 

3. Their interpretation may be a 
mistaken one, in that tumours 
or effusions, etc., may displace 
the heart, its apex beat, and 
cause transmitted pulsation and 
bulging. 

Auscultation is interfered with by 
much the same circumstances 
as the other methods. But, in 
addition, we have to differen- 
tiate heart sounds from those 
of pericardial, pulmonary, and 
pleural origin {vide p. 127). 



Inspection. — The apex beat may 
be seen displaced outwards, or 
downwards and outwards. A 
lifting of the whole cardiac area 
of the chest may be seen at each 
beat, or possibly a persistent 
bulging. 

Palpation. — The displacement of 
the apex beat may be felt, as 
well as the heaving. If a thrill 
is felt it is also a suspicious sign, 
and must be noted. 

Percussion.— There will be in- 
creased area of cardiac dulness, 
both absolute and relative. 



Auscultation will confirm other in- 
dications, or decide by itself the 
position of the apex beat. If 
bruits of organic origin {vide 
p. 129) are present, and known 
to have been so for some time, 
the presence of a heart larger 
than usual is at once certain. 
If no bruits are present the 
character of the two sounds 
must be noted. They are 
chiefly of use to separate pure 
hypertrophy from dilatation or 
failure. 

If by these means we have ascertained that a large heart is 
present, the only other problem requiring solution is this : Is it 
capable of continuing to do its work or not ? 

In by far the greater number of cases, the answer is obvious at 
a glance. The symptoms of failure are too obtrusive, or, on the 
other hand, the absence of such symptoms is quite complete ; but, 
excluding the extremes, we meet with many cases in which the 
most careful attention to every feature may still leave us in doubt. 



124 DIFFERENTIAL DIAGNOSIS chap. 

Such, for example, as a young woman, possibly pregnant too, com- 
plaining of some puffiness of the ankles at night, and we find her 
anaemic and the possessor of a mitral bruit (the relative shares of 
anaemia and heart and pregnancy require much consideration) ; or, 
again, an elderly patient with renal trouble complaining of short- 
ness of breath — Is it cardiac or renal, is the heart beginning to fail ? 
By attention to the following considerations we shall not com- 
plete our diagnosis, but we shall at least get a strong body of evi- 
dence condemning or acquitting the heart of being particeps 
criminis : — 

Inspection \ Will none of them help us much. They will reveal fre- 
Palpation > quency and irregularity, but these are much better deter- 
Percussion ) mined by auscultation. 

Auscultation will give us accurate information on — 

i. Frequency of Pulse. — It is not the absolute frequency that is 
of so much importance. A weak and failing heart may be either 
slow or frequent, fatty hearts are often slow, and sound hearts 
often beat over 90 per minute. What is of importance is the 
rapidity with which the heart settles down after a temporary in- 
creased frequency. The patient should be made to exert himself 
smartly for a few moments, and then the number of beats in the 
next four or five quarters of a minute should be registered and com- 
pared. If the muscle is good the numbers will rapidly diminish 
with each succeeding fifteen seconds, till the rate is regained which 
was previously present. If the increased frequency continues it is 
a suspicious circumstance against the muscle. 

2. Irregularity of Beat in a large heart is very suspicious, and if 
due to muscle failure will, I believe, be invariably associated with 
grave features which cannot be misunderstood. It is only in hearts 
of average size that its indication is doubtful, and then, I think, it 
makes one suspect the nerves rather than the muscle in any case 
where there is room for genuine doubt as to the presence of heart 
failure {vide pp. 117 et seq.). 

3. The Character of the Sounds. — If the natural heart sounds be 
replaced entirely by bruits we lose the assistance they usually afford 
us, and we must rely all the more upon the regularity of the beat 
and other indications. If they be not thus entirely lost, but are 
audible with greater or less distinctness, it must be borne in mind 
that, with an increase in bulk of healthy muscle, there is an increase 
in the contrast between the first and second sounds. The first 
sound is lengthened, and the second sound made sharper. As the 



iv DISEASES OF THORACIC ORGANS 125 

muscle becomes unhealthy or fails in power this contrast becomes 
less, and we may lay down the rule — " The more the first sound 
approximates in character to the second, the more do we fear that 
hypertrophy is being overtaken by dilatation or weakness." If the 
first sound is very weak, almost inaudible, this is, excluding fallacies 
of emphysematous lung, etc., a sure sign of failing muscle. 

General Symptoms. — We can only repeat again that back pressure 
effects, if definitely present, are essentially signs of failure. Their 
absence or amelioration is provided for by hypertrophy, and hence 
they conclusively prove by their presence that the muscle is feeling 
the strain. 

We may now, with these views of hypertrophy and dilatation, 
briefly examine the elements of the problem, " How is the heart 
itself affected by various valvular affections ? " 

, T , . , f Competent. 

Valves must be { T r , _ , . . ., .. 

\ Incompetent, j Relative, from too wide an orifice. 



Absolute, from intrinsic disease 
(thickened, puckered, etc.). 

Orifices must be 1. Correctly adapted for their valves. 

2. Narrowed (by adhesions). 

3. Too large (by dilatation of chamber). 

A moment's consideration of any single valve trouble will at 
once show that any pathological change in the structure or orifice 
leading to the leakage or stenosis must throw extra work on to that 
chamber which (reckoning from the direction of the blood stream) 
immediately precedes the lesion, and hence we might infer that 
hypertrophy should be the immediate result. But as the extra 
work is thrown on to the chamber at very different periods in its 
cycle of work and rest, the results are not quite the same in the two 
cases. In pure stenosis the extra strain comes during systole when 
the muscle is expecting to work, and here we can easily understand 
that almost pure hypertrophy results. In simple incompetency of 
a valve, however produced, the strain comes on the precedent 
chamber at a moment when the muscle is relaxing or resting, and 
hence, being caught unawares, so to speak, it is likely to yield 
somewhat, and an increase in the volume of the cavity is likely to 
ensue, or dilatation in its first sense, and, unless compensating 
energy or strength appears, dilatation in the second sense will soon 
appear. This precedent chamber (in incompetency at any rate) 
contains a larger quantity of blood than usual, which will, in systole, 
be forced into the succedent chamber at a time when it is relaxing 



i26 DIFFERENTIAL DIAGNOSIS chap. 

or resting, and hence in this chamber, too, there must occur some 
degree of dilatation to be again compensated by hypertrophy. 
When two or more valves are affected, and possibly in different 
ways, the problem becomes more difficult to follow, but the above 
principles will help us, provided we have the data as to time and 
amount of the several affections. Such data are, however, practi- 
cally never offered to us, and we have to be content with accepting 
the general clinical result that in all cases of chronic valvular disease 
of the heart the organ becomes larger in its dimensions as ascer- 
tained by physical examination. This enlargement is nature's effort 
at compensation, and when the hypertrophy reaches its limits, or 
the muscle from any cause becomes badly nourished, cardiac failure 
and serious symptoms will supervene, whatever be the actual capa- 
city of the chambers. 



CARDIAC BRUITS, AND SOUNDS THAT MAY BE 
MISTAKEN FOR THEM 

If, on auscultation of a chest, an abnormal sound be heard in 
the cardiac or aortic region, the first point to determine is, whether 
its origin lies in the cardiac or pulmonary organs. This, as a rule, 
is not difficult to decide. Pleuropericardial friction sounds re- 
sembling a pericardial rub, and compression of a small portion of 
lung tissue by the heart's movements, with a noise resembling a 
short systolic bruit, are the chief difficulties. 

In the first place, they will either of them only be heard locally 
where they arise, somewhere along the margin of the heart. This 
and their rough character will alone be sufficient to separate them 
from endocardial bruits, which are heard over the bulk of the heart, 
and always conducted at least a little way from the point of maxi- 
mum intensity. Then if by making the patient hold his breath for 
a few seconds the sound entirely ceases, we know at any rate that 
the inside of the pericardium is free from acute inflammation, and 
this is the most important clinical point, for an acute pleurisy here 
is only of additional importance from the liability to spread to the 
inner surface of the pericardium. If the sound does not entirely 
disappear on holding the breath, the heart movements must take 
some share in its production. Probably the pericardium is adherent 
to the heart on the one hand, and the pleura on the other. The 
position in which such sound is heard, on the boundary or just out- 
side the limits of the heart, and a history of previous pericarditis or 



DISEASES OF THORACIC ORGANS 



127 



pleurisy, will help us in deciding pleura v. pericardium, though 
frequently it is quite impossible to decide the point. Nor is the 
decision of very great importance practically, for either solution 
suggests adhesions which may in the long run interfere with the 
cardiac muscle, and are consequently to be feared in the future. It 
is well now to make the patient hold his breath — first at the end 
of deep inspiration, and secondly at the end of deep expiration. 
Should the abnormal sound be heard at one of these periods, and 
entirely disappear at the other, or, at least, be materially altered in 
character and loudness, it is probable that it depends on the 
forcible emptying of a small tongue of lung tissue by the mechanical 
pressure of the heart in systole. This is, however, a rare sound to 
hear. 

If we have thus decided that the sound has its origin in the 
cardiac organs, the next point is to determine whether it is peri- 
cardial or endocardial. At the apex of the heart very little diffi- 
culty will be experienced, for the to-and-fro rubbing of pericarditis 
present throughout the whole cycle of the heart's action is very 
unlike any apical endocardial bruits, and the galloping rhythm of 
a rapid heart only requires a little careful listening to distinguish 
it. At the base, where pericardial bruits are perhaps more common, 
the difficulty of distinguishing them from double aortic murmurs is 
a little greater. 

The following table correlates and contrasts the most important 
distinguishing features in all cases : — 



Exo- or Pericardial Sounds. Endocardial Sounds. 



Character. 



Time of occurrence. 



Conduction. 



Almost always a fric- 
tion or rubbing 
sound ; practically 
never musical. 

At any period of cycle, 
not specially with 
systole or diastole. 

Are not conducted 
along the blood 
stream or to apex, 
though they may be 
heard over a wide 
area. 



More usually blowing 
in character ; often 
musical. 

Always in connection 
with, if not actually 
at, systole or dia- 
stole. 

Conducted upwards, or 
to the apex and 
axilla, except pre- 
systolic bruits, which 
have such special 
characteristics as to 
barely allow of mis- 
takes. 



128 



DIFFERENTIAL DIAGNOSIS 



Exo- or Pericardial Sounds. Endocardial Sounds. 



Position of maximum 
intensity. 



Effects of pressure. 



Variation from day to 
day. 



Pulse and associated 
symptoms. 



May be heard any- 
where, but where 
heard do not gradu- 
ally lose in intensity 
on gradual shifting 
of stethoscope. 



In yielding chests firm 
pressure is likely to 
cause marked altera- 
tion in sound. 



Probably vary in area 
from day to day, and 
may disappear 
rather rapidly, but 
do not dodge about, 
appearing and dis- 
appearing alter- 
nately. 

Pulse rate sure to be 
accelerated in acute 
pericarditis (in chro- 
nic cases no rub 
because of adhe- 
sions, or if present 
is pleuropericardial, 
vide supra). 



Apex, for mitral bruits, 
base or mid ster- 
num, for aortic bruits, 
are points of maxi- 
mum intensity, and 
the bruits gradually 
diminish from their 
point of greatest 
distinctness. 

Pressure makes no real 
difference in the 
sound, though the 
closer fit of the 
stethoscope may en- 
able it to be heard 
more distinctly. 

More likely to be con- 
stant, except in recent 
or ulcerative endo- 
carditis ; they have 
at times a curious 
habit of appearing 
and disappearing in 
a most capricious 
manner. 

Pulse rate entirely 
dependent on the 
recentness of the in- 
flammatoryattack or 
on physical condition 
of patient, so that 
in chronic cases it 
may be for years 
quite natural. 



Considerable precision may thus enter into our decision as to 
whether the source of an abnormal sound is endo- or exocardial, 
but when we come to consider the various problems connected 
with unusual sounds of endocardial origin, we are on very treacher- 
ous ground indeed. We can now and again decide some of them 
with a tolerable degree of accuracy, but on other occasions and 
for other problems even the keenest judgment of the most mature ex- 
perience will only with diffidence and hesitation express an opinion. 



DISEASES OF THORACIC ORGANS 



129 



Epitomised and tabulated the position is this : — 

1. What is the exact origin of the bruit ? 

Blood states, poverty of blood, either of quantity or quality. 

Organic disease of' . 

, , . I Mitral 

valves obvious to . 
,, 1 j Aortic, 

the naked eye on L , 
nncf ^^^^ Q ^ I pulmonary 
Tricuspid 



It may be 
due to 



post - mortem 
amination. 



(Insufficiency or sten- 
osis, recent inflam- 



mation or effects 
of old trouble. 



I Leakage of valves'! 

without naked eye J-May be due to 
changes. } 

Aneurysm. 



General dilatation of 
walls of cavities, or 
improper or feeble 
action of individual 
musculi papillares. 



2. What is the vital significance to the patient of the bruit 
thus detected? 

Here I shall attempt only a complete solution of some of the 
simpler problems, with an indication of the principles that must 
guide us in attempting to decide the more complex ones. 



A.— WHAT IS THE EXACT ORIGIN OF THE BRUIT? 
(a) Hcemic v. Organic Bruits 

It is usually comparatively easy to determine whether a bruit is 
due to poverty of the blood — ordinarily termed hsemic bruits — 
though the precise cause of such bruits is a matter of very great 
dispute and uncertainty ; Dr. Byrom Bramwell offering us a choice 
of (1) pulmonary, (2) mitral, (3) left appendicular. Whatever its 
cause, the following particulars will suffice to separate it from 
bruits owning a definite organic lesion as causative factor : — 



Position. 



If of Haemic Origin. 
Rarely heard at the 
apex, and if so, not 
conducted into axilla ; 
usually heard at the 
base, and better a little 
to the left of the ster- 
num. 



If of Organic Origin. 
Heard at apex, and often 
conducted into axilla ; 
basic organic bruits are 
almost always better 
heard a little to the 
right of the sternum ; 
pulmonary organic 
bruits being rare, ex- 
cept as congenital con- 
dition. 



3° 



DIFFERENTIAL DIAGNOSIS 



Time. 

Character. 

Conduction. 



Loudness al- 
tered. 



Associated con- 
ditions. 



If of Hsemic Origin. 

Always systolic, never 
diastolic or presys- 
tolic. 

Not very distinctive, but 
they are never regu- 
larly musical. 

Rarely conducted any 
distance beyond their 
point of maximum in- 
tensity; somewhat sud- 
denly cease to be heard 
as stethoscope is moved. 

Become very much louder 
on patient lying down 
on the back. 



Patient obviously anaemic, 
and as this improves, 
the bruit is likely to 
disappear. 



If of Organic Origin. 

May be, of course, sys- 
tolic or diastolic, or 
both, or presystolic. 

May be musical. 



Usually conducted some 
way from maximum 
point, and gradually 
die away in intensity as 
stethoscope is shifted. 

Not markedly altered by 
patient lying on the 
back ; any alteration 
usually in direction of 
diminution. • 

Not necessarily anaemic ; 
aortic disease is most 
likely to cause anaemia. 
This anaemia is not 
likely to yield to treat- 
ment, and if it does, 
the bruit still persists. 



(b) Valve of Origin of Bruits of Organic Origin 

The rules commonly laid down for discriminating the various 
sources of bruits due to organic valvular trouble may be briefly 
indicated as follows : — 



Mitral systolic, indi- 
cating regurgita- 
tion through an in- 
competent mitral 
valve. 



Mitral presystolic, 
indicating abnor- 
mal narrowing of 
mitral orifice. 



Systolic in time, i.e. accompanying or replacing 
the first sound ; best heard at the apex, con- 
ducted into the axilla even to the angle of the 
left scapula ; pulmonary second sound usually 
accentuated ; apex beat displaced down and 
out in old standing cases, indicating some 
degree of enlargement of the left side the 
heart ; pulse small. 

Presystolic in time, leading up to a sharply 
ceasing first sound ; best heard a little above 
the apex, not conducted very far from its 
point of maximum intensity ; pulmonary second 



DISEASES OF THORACIC ORGANS 



131 



Aortic systolic, indi- 
cating obstruction 
at aortic orifice. 



Aortic diastolic, in- 
dicating incompe- 
tent aortic valves. 



Tricuspid systolic, 
indicating regurgi- 
tation through in- 
competent valves. 



sound very accentuated ; apex beat if dis- 
placed at all, chiefly to the left — outwards — 
indicating enlargement of the right side. (If 
the word ' abrupt ' be pronounced with a very 
rolling r the word becomes almost onomato- 
poeic of the phenomena to be appreciated in 
connection with this bruit.) 

Systolic in time, best heard over mid sternum 
about the third cartilage, or in the second 
right space ; conducted upwards towards the 
vessels of the neck ; apex beat displaced in 
old cases farther down and out than with any 
other bruit, indicating the greatest hyper- 
trophy of the left ventricle ; pulse small. 

Heard with or replacing the second sound, best 
over mid sternum opposite the third cartilages 
or in second space on the right ; conducted 
down to the apex or to the ensiform cartilage, 
and so conspicuously as to be sometimes best 
heard at those spots ; apex beat displaced 
down and out, again indicating a great degree 
of enlargement of the left ventricle ; pulse 
peculiarly collapsing — the water-hammer or 
Corrigan's pulse. 

Systolic in time, best heard over the right ven- 
tricle, and conducted a little outwards to the 
right ; very rare except in the later stages of 
heart failure, and is accompanied with a venous 
systolic pulse in the neck ; indications of 
hypertrophied right ventricle pushing apex 
beat outwards. 

Best heard to the left of the sternum, very rough ; 
conducted upwards to the left. 

Too rare to notice here. 



Pulmonary systolic, 
or stenosis of pul- 
monary orifice. 

Pulmonary diastolic ; 
tricuspid presys- 
tolic. 

In many cases, if used with discrimination, these rules will give 
tolerably accurate results, and are sufficiently useful to be remem- 
bered ; but even in the most competent and careful hands they 
are apt to mislead, for statistics have shown x that " out of every 
hundred hearts we listen to, in thirty-six the bruits will give us 
exact information, in ten they will lead us absolutely astray, and 

1 Thesis for M.D. Oxon. based on some 700 autopsies. 



132 DIFFERENTIAL DIAGNOSIS chap. 

in fifty-six they will give us information in excess or defect of the 
truth." The matter is of less importance, as we must iterate and 
reiterate the fact that every heart, with (or without) bruits, has to 
be judged on the merits of its muscle power and energy, and not 
by the bruits, the patient's condition must be taken as we find it, 
and not as one deducible from a theory of what it ought to be by 
the murmurs present. Of all factors by which our clinical judg- 
ment is influenced, that of the bruits present is the one of smallest 
weight. 

The above rules will equally apply to bruits arising under cir- 
cumstances which lead us to think that they are more likely due to 
relative incompetency or muscle imperfections, such, for instance, 
as a case in which cardiac failure is already noted, and a bruit 
becomes audible, unexpectedly developing under observation without 
pyrexia. The pathology of such cases will be touched on a little 
further in a subsequent section (vide pp. 135 et seg.). 

(c) The Bruits of Aneurysm v. Valvular Disease 

We have already(pp. 105 etseq.) dealt with the separation of aneu- 
rysms from intrathoracic solid tumours ; we have here to separate 
them from lesions of the heart itself. Aneurysms of the transverse 
or descending aorta can scarcely give rise to suspicion of valvular 
mischief. The tumour and bruits and other local indications are 
too far removed from the situations where enlargement of the heart 
or valvular bruits would be observed. It is those of the ascending 
arch that require some care in discrimination, though even here 
the presence or absence of implication of the valves is of more 
importance than the presence or absence of an aneurysm as such. 

The bruit of aneurysm is most The bruit of valvular disease is 
frequently systolic, only occa- most frequently double, occa- 

sionally double, practically sionally systolic or diastolic 

never diastolic only, often also only (very rarely found to have 

absent altogether ; rarely con- been completely absent when 

ducted very far, and never down post-mortem shows gross valvu- 

the sternum. lar disease) ; usually conducted 

a good distance, and often 
heard down the sternum or at 
apex of heart. 

Then the question of associated cardiac enlargement must be 
considered. My experience in the post-mortem room, in agree- 



iv DISEASES OF THORACIC ORGANS 133 

ment with recent observations, tends to show that aneurysms as 
such, i.e. when so situated as not to interfere with the aortic valves, 
have but little influence in causing hypertrophy of the heart. Aortic 
valve disease, on the other hand, is the especial trouble pre-emi- 
nently calculated to produce hypertrophy and dilatation of the left 
ventricle ; hence, if with the bruit there is well-marked enlargement 
of the heart, the probabilities are strongly in favour of valvular 
disease ; if there is but little or no evidence of such enlargement, 
the probabilities are in favour of an aneurysm as the cause of the 
murmur. Again, if there be a dulness extending suspiciously to 
the right of the sternum, the position of the heart's apex beat will 
give us help. Should this be displaced outwards much more than 
downwards, it is probable we have to deal with an enlarged right 
ventricle (lung trouble or mitral stenosis) ; if much downwards as 
well as outwards, aortic valve trouble is again probable. If not 
very materially displaced, aneurysm again is strongly suggested (or 
solid tumour). 

It has to be admitted that the general conditions, viz. severe 
physical exertion over long periods, alcoholic excess, syphilis, 
advanced age with senile degeneration, renal disease, etc., which 
are predisposing factors in aneurysm, are equally the predisposing 
factors in primary aortic valve disease (the valves are, in fact, 
merely a part of the aorta, and degeneration with aneurysmal yield- 
ing may occur at any point), so that it is by no means an unfrequent 
thing, in fact I think it is a rule of the majority of cases, that when 
aneurysm occurs it shall be associated with valvular lesions, and 
hence it is frequently impossible to exclude the aneurysm, although 
we have positive evidence that the heart is affected. The diagnosis 
is of less importance in that the condition is a grave one, and what 
is likely to help the heart is likely to help the patient to bear with, 
or to cure the aneurysm if it exists. 



B.— WHAT IS THE VITAL SIGNIFICANCE TO THE 
PATIENT OF THE BRUITS? 

This includes two problems, the first of which, viz. the bruit as 
an indication of the condition of the muscle of the heart, has really 
more to do with prognosis than diagnosis ; it has already been 
touched upon in dealing with the symptoms that suggest morbus 
cordis, and will be further considered {vide pp. 1 3 5 etseq.); the second 
is the bruit as a direct indicator of leakage or stenosis, and the 



i 3 4 DIFFERENTIAL DIAGNOSIS chap. 

influence of these on the patient's condition ; this we will now con- 
sider. 

Bruits of hsemic origin may certainly be ignored in cardiac 
pathology. They are accidental phenomena in diseases of other 
origin, and disappear with the disappearance of the blood dys- 
crasia, and their significance is nil beyond the significance of this 
dyscrasia. 

Bruits of aneurysmal origin, too, have the significance of the 
aneurysm itself. They add nothing to our knowledge of the course 
the arterial disease will take ; they give no guidance in treatment, 
and their disappearance, if they do disappear, does not necessarily 
mean the cure or amelioration of the condition. This work does 
not deal with treatment, but I cannot refrain from putting on 
record an emphatic protest against any extremes of active treatment 
in aortic aneurysms, such as starvation and severe bleedings. The 
lesion is one that will kill quite fast enough without our assistance, 
and our efforts had better be directed to making life bearable by 
counsels of moderation in all things than to rendering miserable 
the remaining years of a threatened life. 

Bruits of undoubtedly organic valvular origin have the following 
significations : — 

(i) To determine the presence of recent inflammation {vide 
p. 116). 

(2) To determine excessive dilatation of a chamber {vide p. 
122). 

(3) By their disappearance to determine muscular weakness 
{vide p. 140). 

(4) To determine single or combined alterations of old stand- 
ing in the valves, with their significance. 

This last (4) is the problem to the decision of which I devoted 
some time ago a very considerable amount of statistical inquiry. 
Omitting the actual figures, the tables I prepared showed that, sup- 
posing the patient died from the effects of heart disease — 

{a) Mitral incompetency gives, amongst single lesions, the 

worst prospect of prolonged life. 
{b) Aortic incompetency also amongst single lesions gives the 

best prospect. 
{c) The question between aortic stenosis and mitral stenosis 

depends on other factors to such an extent that the 



iv DISEASES OF THORACIC ORGANS 135 

isolated lesion is of very small importance, and probably 
the prospects are about equal. 

(d) If aortic stenosis be combined with mitral incompetency, 

the patient gains about three and a half years of life from 
what he would enjoy with aortic stenosis only. 

(e) Mitral stenosis combined with aortic stenosis is a very fatal 

combination ; but if the pulmonary or tricuspid be also 
stenosed, the patient gains about seven years of life. 
Such a marked difference points strongly to the lung as 
the weak spot in heart disease. 

These results, at any rate the first one (which seemed to be the 
most firmly established by figures), are so startling and so contrary 
to what is apparently one's general experience of the innocuousness 
of a mitral systolic bruit, that I was then (1890), and still am, driven 
to the conclusion that they illustrate more forcibly than any other 
argument the futility of attempting to lay any weight on the nature 
of the bruits in estimating the value or power of a heart whose 
valvular machinery is damaged. I leave them, without further com- 
ment, to be refuted or corroborated by future investigators. 



HEART DISEASE IRRESPECTIVE OF MURMURS 

In discussing hitherto the pathology of cardiac disease and 
hypertrophy and dilatation, we have had in mind chiefly chronic 
organic disease of the valves as the essential cause of the disturb- 
ance. It is certain that the nervous and muscular mechanisms, 
connections, and structures are capable, in an otherwise fairly 
healthy individual, of obviating to an almost complete extent, and 
for a very long time, such defections in valve arrangements ; but if 
the patient is to die, as many do (though very many do not) from 
chronic valvular trouble, a time eventually arrives for him when 
such compensation fails from malnutrition or overstrain of muscle 
(? of nerve too). The case then, from its causation, goes into a 
special group, but from its clinical features remains an illustration 
of the class of cases which we must now consider, viz. those in 
which the nervous or muscular mechanisms have broken down, or 
possibly (as in valvular trouble ?) both have given out. The precise 
pathology of the various examples of this class is often most obscure, 
and probably the essential elements in it vary from time to time, 
now nerve, now muscle being at fault. So far as can be understood, 



136 



DIFFERENTIAL DIAGNOSIS 



Muscular defects 
of degeneration 
(whether fatty 
or fibrous or 
other is not 
very material ; 
the muscle is 
no longer nat- 
ural). 



Of slower onset 
through months 
and years. 



I think the following table represents fairly completely the causes 
which may be at work in producing the clinical features of the case : — 

Malnutrition from the circulat- 
ory disturbances in the heart 
itself, of valvular disease ; 
common. 

Malnutrition from more general 
conditions, e.g. age, vascular 
degeneration, kidney disease, 
gout, obesity, etc. ; common. 

Definite new growths, syphilis, 
tubercle, malignant disease, 
hydatids, etc. ; all are rare. 

Fibrosis or scar formation from 
any cause, especially peri- or 
endocarditis, syphilis, etc. ; 
also common, at any rate as 
revealed by the microscope. 
' Acute febrile disease, especially 
perhaps pneumonia, typhoid, 
and septicaemia (from pyrexia, 
or toxins, or both). Poisons, 
such as tobacco, alcohol, etc., 
which may affect the muscle 
as well as the nerves. (This 
group may come on more in- 
sidiously.) 

From diseases of any organ, 
e.g. intestines, stomach, ovary, 
etc. (? thyroid). 

Pressure on peripheral part of 
nerves, enlarged glands, e.g. 
central pressure of tumours, 
meningitis, etc. 

Loss of control of nerves from 
actual neuritis or smaller de- 
gree of nerve illness. 

Poisons — tobacco, alcohol, prob- 
ably thyroid secretion, etc. 
Diphtheria, influenza, and 
other specific diseases prob- 
ably should also be placed 
here. 



Nervous influ- 
ences or de- 
fects. 



Of more rapid 
onset, possibly 
days or weeks. 



Purely reflex. 



Direct effects on 
vagi or acceler- 
ators. 



iv DISEASES OF THORACIC ORGANS 137 

The clinical features of the cases are as varied as the possible 
causations. Sometimes they assume the shape of the most dangerous 
and serious illnesses we can meet with ; sometimes, on the other hand, 
they indicate but a trivial malady ; yet the former may prove of no 
moment, while sudden death may terminate the latter. They may 
present all the general indications of back pressure, or they may 
confine themselves almost entirely to local pain and distress. Diag- 
nosis becomes increasingly difficult with the absence of indubitable 
signs of organic disease, and mistakes must constantly occur even 
to the most experienced. Still, a careful inquiry into the history of 
the case, and an equally careful weighing and balancing of all avail- 
able factors must be undertaken, and will help us materially in, at 
any rate, basing our opinion on a sound foundation of probability, 
beyond which clinical medicine can rarely go ; certainty is rarely 
attainable where the exceeding delicacy of ill-understood physio- 
logical balances is in question. 

It may be laid down as a general rule (not perhaps without some 
very grave exceptions — vagus neuritis, for example, after diphtheria) 
that affections of the nerve apparatus are less serious in their 
outlook than those of the muscle. Remembering how easily the 
heart beat is affected, at least in frequency, by every passing 
mental shock, by pain, by gastric disorder, by, in short, reflex in- 
fluences from every quarter, the general truth of this rule in practice 
must, I think, be accepted. Hence our first efforts at diagnosis 
should be directed to an endeavour to determine on which side 
weakness lies. The following paragraphs in parallel columns will 
show the points of distinction more clearly, and bring them into 
sharper contrast. 



DERANGEMENTS OF THE DERANGEMENTS IN THE 

NERVOUS CONTROL MUSCLE APPARATUS 

Points in the Previous History 

If previous attacks of symptoms Previous attacks of symptom have 
have occurred, they have prob- probably not cleared up entirely, 
ably cleared up entirely, leaving but have left permanent short- 
no trace of permanent and per- ness of breath or other evidence 
sistent signs of ill-health. They of ill-health. They were prob- 
were not associated with decided ably associated with definite 
evidence of back pressure effects. signs of back pressure. In 



38 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



The first attack was probably 
associated with some mental 
shock or dyspeptic trouble, or if 
with a definite illness, it was 
more likely influenza or diph- 
theria (both known to cause 
nerve changes) than rheumatism 
or scarlet fever, etc. (known to 
produce endo- or myocarditis). 
Attack more likely to be quite 
sudden in onset, without obvious 
exciting cause. 



young people the first attack 
traceable to rheumatism or other 
disease known to produce organic 
changes in endo- or myocardium. 
In elderly patients there will 
probably be found an admission 
of progressive feebleness and 
shortness of breath previous to 
an actual attack of symptoms 
calling for medical aid. 



Points in the Symptoms Complained of 



More likely to be stress laid on 
the local symptoms, pain more 
or less sudden and spasmodic in 
the cardiac area (rapidly sub- 
siding after eructations or vomit- 
ing), palpitation, fluttering sen- 
sations, choking, etc., also pro- 
minent, but soon subsiding. 
Likely enough to return on a 
repetition of the recognised 
cause, e.g. heavy meal, tobacco, 
alcohol, etc. Faintness is again 
a very common phenomenon in 
such cases, but fatal syncope 
extremely rare. 



Local symptoms less prominent, 
and usually masked by the 
general distress. If they are 
prominent there is no doubt 
about their genuine severity 
(angina, vide p. i 1 3 ), and they do 
not subside suddenly after mere 
eructation or vomiting. Exciting 
cause much more frequently 
physical exertion of some kind, 
or very violent excitement. 
Faintness of an ordinary char- 
acter is not common, but fatal 
syncope is fairly frequent. 



Points ascertained by Examination of the Patient 

General Considerations and Conditions 

Age. — In the young the two great causes of cardiac muscle 
weakness are valvular trouble (congenital or acquired) and acute 
pyrexial disease. If these two can be excluded, cardiac complaints 
in younger subjects are almost certainly nervous in origin. In 
older patients, when their complaints may point to a cardiac source, 
we are much more anxious about the condition of the muscle. 
This anxiety will be increased very much by evidence of renal 
disease or arterial degeneration. The latter, in fact, is a better 
gauge of age than the calendar's tale of years. The coronary 



iv DISEASES OF THORACIC ORGANS 139 

arteries so frequently share in this degeneration that a degenerate 
radial or temporal is an absolute bar to our regarding lightly any 
history of cardiac attacks ; they compel a serious view being 
taken of such a case. Fatal angina or an aneurysm, otherwise 
undiscoverable but with a gloomy outlook, must inevitably occur to 
our minds under such circumstances. In later life, too, one is 
inclined to look more favourably on the same symptoms in a woman 
than in a man. 

Sex. — Of sex, apart from age, but little can be said. Women, 
as a rule, are certainly more liable than men to view with appre- 
hension slight symptoms or disquieting sensations in the cardiac 
region ; hence, if there is no obvious origin for heart disease, one 
would be more inclined in a woman towards a neurotic explanation 
of a case. If, on the other hand, obvious hysterical manifestations 
of other kinds are present — Grave's disease, influenza, tobacco, 
alcohol, sexual indulgence, masturbation, puberty with its strain on 
the system, a neurotic heredity — if anyone of these gives us a clue, 
sex at once becomes of very little account in comparison with such 
indication. 

Back Pressure Effects. — These we have already (p. 118) considered 
in some detail. For our present purposes we may divide them into 
— (1) disturbances of function; (2) disturbances of structure — 
oedema, fibrosis, etc. — and we may state that — 

In nervous affections of the heart In muscular troubles both classes 

the latter class is seldom are common, and, indeed, the 

(? never — vagus neuritis, for characteristic feature. Provided 

example) seen. Evidence of there is no local cause for a 

the former class is fairly com- member of the second class, its 

mon : shortness of breath with- occurrence is practically patho- 

out rales or bloody expectora- gnomonic of heart muscle failure, 
tion, disturbances of general 
cerebration, or of special senses, 
or irritability of stomach, etc. 

Local Examination of the Cardiac Region 

Inspection, palpation, and percussion are only of essential utility in 
determining the presence or absence of hypertrophy and dilatation, 
and as one indication of frequency and irregularity. 

Hypertrophy and Dilatation, either or both 

In purely nervous affections of the In muscular troubles alteration in 
heart the organ is but rarely the size of the heart is constant 



140 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



much larger than normal. The 
chief exception is long-standing 
Grave's disease. 



except in acute febrile disorders 
(on the presence of which the 
diagnosis mainly rests). This, 
in fact, when marked, constitutes 
the type case. 



Frequency and Irregularity 



Tachycardia and bradycardia are 
the commonest features in 
nervous affections of the heart. 
In fact, either of them, possibly 
with some irregularity, but with- 
out other objective signs of heart 
disease, constitutes the type case, 
and under such circumstances, 
in combination, a pulse of over 
160 or under 50 may safely be 
regarded as due to nervous in- 
fluences. 



Tobacco in excess, Grave's disease, 
influenza are the common causes 
of such tachycardia and palpita- 
tion, and careful inquiry must 
be made for them. 



In the more slowly developing 
defects of muscle, frequency 
rarely rises much beyond 130 
without at the same time being 
associated with marked tumul- 
tuous irregularity and signs of 
back pressure ; nor, on the 
other hand, is it often reduced 
below 60 without similar indica- 
tions. In the more rapidly 
developing muscle failure of 
poisons and pyrexia frequency 
may be very high without such 
other symptoms, but then the 
feebleness of the sounds is our 
best guide. 

Irregularity alone as the sole indi- 
cation of muscular trouble never 
occurs, at any rate for long. 
Should it be the first warning 
others will very soon appear. 



Vide frequency also (on p. 124) under Hypertrophy and Dilata- 



tion. 



Bruits. — In nervous troubles bruits 
of any kind are exceedingly rare, 
and still rarer is it to find one 
that follows the rules laid down 
for those of valvular origin, 
though I think it probable that 
some of the obscurer murmurs 
may be due to irregularity of 
nerve influence on individual 
muscle bundles. 



The presence of bruits in muscle 
troubles has already been dis- 
cussed (p. 116). Here we need 
only mention that the disappear- 
ance of a valvular bruit with in- 
crease in severity of symptoms 
is pathognomonic of muscle 
failure, as, indeed, is its first 
appearance under such cir- 
cumstances of increase in symp- 
toms. 



DISEASES OF THORACIC ORGANS 



[41 



The Ordinary Cardiac Sounds 
Nervous affections of the heart Muscle troubles, on the other hand, 



have a peculiar tendency to 
render the sounds sharper and 
more distinct as noises, though 
the contrast between the first 
and second may be lost in ex- 
treme frequencies. If any sound 
disappears in nerve troubles it 
is the second. 



have a tendency to shorten the 
first sound, and, at the same 
time, to render it less audible. 
So much so, that in some cases 
of poisoning, prolonged pyrexia 
(as in typhoid, etc.) or fatty 
heart, the first sound may be- 
come almost inaudible. This is 
true whether bruits are present 
or not. Their presence only 
renders its appreciation more 
difficult. 



Such, in detail, are the individual points requiring attention in 
the diagnosis of the nature and meaning of cardiac complaints. In 
practice the difficulty lies not so much in estimating these sepa- 
rately as in weighing them collectively and striking a balance 
between those which point in opposite directions. It is here that 
clinical experience and acumen have their most brilliant oppor- 
tunities for making a reputation for their possessor, and no hard 
and fast rules can replace them. The only advice I have to give of 
general application is, " Don't be in too great a hurry to express a 
decided opinion. Time and circumstances will often throw a clear 
light on a case which is at first apparently obscure and perplexing." 



ULCERATIVE ENDOCARDITIS 



To understand the diagnostic problems of ulcerative endocarditis 
it is necessary to enter into the outlines of the pathology of endo- 
carditis in general. The four following postulates constitute the 
essential foundations : — 

1. That acute endocarditis arises, precisely like inflammation 
elsewhere, as the result of an irritant applied to the membrane. 

2. That the severity of the anatomical lesions, produced by the 
inflammation, is strictly proportionate to the relative strength of — 
on the one side, the toxicity or nature of the irritant ; on the other 
side, the resisting power of the membrane. 

3. That in clinical practice the irritant is always either chemical 



i 4 2 DIFFERENTIAL DIAGNOSIS chap. 

substances produced by (i) unnatural metabolism of the tissues, 1 
(2) microbic activity, or it is the microbes themselves and their 
activities locally exerted on the membrane. 

4. That a previously damaged valve forms a locus minoris 
resistentia to the influence of any poison circulating in the blood. 

In connection with postulate (2) and our knowledge of the 
anatomical changes that ordinarily accompany any inflammatory 
process, we may tabulate endocardial changes thus : — 

Phenomena of constant Phenomena whose occurrence depends on 
occurrence at the circumstances denned by postulate (2). 

onset in every case 
of acute endocarditis. 

\d) Simple swelling without loss of epithelium, 
no vegetations, and ultimately complete 
resolution. 

Active congestion, with \{b) Swelling plus loss of epithelium (micro- 
effusion of serum and J scopic ulceration) ; appearance of vegeta- 
cells and swelling of \ tions ; ultimately some thickening or 
the valve. J scarring left behind. 

'(c) Swelling, loss of epithelium, vegetations 
plus loss of other tissues and naked eye 
ulceration. 

(a) Must be allowed to occur in those cases of rheumatic fever 
and other illnesses in which a definite valvular bruit occurs, but 
finally entirely disappears. 

(b) Is the most common clinical occurrence in such illnesses 
(rheumatic fever) as leave a permanent organic valvular bruit. 
These must in strictness be also termed ulcerative endocarditis, 
but as the loss of tissue is of microscopic proportions, the term is 
usually reserved for the third class. 

(c) It is to this condition that the term ulcerative endocarditis 
is usually applied. I have put it in serial continuity to the other 
forms to emphasise what I believe to be its real position, viz. an 
endocarditis, the severity and course of which depend upon circum- 
stances which may be called accidental, in support or explanation 
of which statement we will now consider the clinical occurrence of 
severe endocarditis. 

First of all, cases of the following type are unfortunately by no 
means rare. A patient, probably under twenty, is attacked with 

1 This is inserted in view of the doubt whether rheumatism is a microbic disease. 



iv DISEASES OF THORACIC ORGANS 143 

rheumatic fever. A valvular bruit develops and persists, but the 
patient becomes more or less convalescent from distinct rheumatic 
symptoms. Then, without any pyrexia, or very slight and tem- 
porary fever, one or other, or perhaps one after the other, some of 
the following incidents occur: attacks of pain in and swelling of 
the spleen, renal pain with haematuria, cough with bloody sputum 
and a pleuritic rub, oedema with loss of circulation in a limb or 
part of one, hemiplegia, etc., each and all evidences of an embolus 
being swept from the heart into the organ specified. The patient 
may yet live on in an invalid condition for some months, and even 
for years, and eventually succumb from cardiac failure or from an 
embolus proving fatal. On autopsy we find the areas of embolism, 
corresponding to the symptoms, each and all in what may be 
termed a quiescent condition, i.e. one the ultimate end of which 
will be simple fibrosis or scarring after absorption of very slightly 
irritating dead tissue. We find on the valves of the heart a greater 
or less amount of vegetations, on the removal of which losses of 
substance — ulcers — may be plainly visible in the valve tissue, but, 
and this is the point, from neither the valves nor the embolised areas 
can any growth of pathogenic microbes be obtained. Such a case must 
be termed severe — and ulcerative — endocarditis, though its origin 
is purely rheumatic. 

Now let us sketch the other form. An attack of rheumatic 
fever, followed by the appearance of a bruit as before, but the 
patient gets quite well of all symptoms and remains so, a murmur 
being the only evidence of his attack. One day an entrance to his 
system is effected by potent -for -evil microbes, and now follows a 
train of symptoms which in gross may be termed septicaemic — 
hectic, sweating, rigors, diarrhoea, ups and downs — and quite 
probably evidences of emboli, as in the previous case. The 
patient dies, not of an apyrexial exhaustion or cardiac failure, but 
evidently of some acute febrile process. On autopsy we find, not 
quiescent, absorbing embolised areas, but the seat of each embolus 
is occupied by a soft, semi-purulent collection of debris, the heart 
valves or endocardium may be in precisely the same condition to 
naked eye as in the previous case — though it is probable that the 
loss of tissue will be more evident — vegetations may or may not be 
equally abundant, but from the ulcer and from each embolised area 
can be obtained a culture of pathogenic microbes. Microbes of many 
kinds have thus been found — gonococci, pneumococci, pyogenes 
albus, p. aureus, etc. 

The difference between the two cases is clinically real enough 



144 DIFFERENTIAL DIAGNOSIS chap. 

and serious enough, though the anatomical changes to naked eye 
may be practically identical, at least in the heart. But the differ- 
ence is, I maintain, a quasi-accidental one, and due to a contamina- 
tion of the blood by virulent microbes, which (vide above) may be of 
almost any kind, and hence ulcerative endocarditis is not a specific 
disease to the same degree as are scarlet fever, syphilis, or small- 
pox, for example. It is more like pneumonia, which can be 
produced also by many microbes. 

Diagnosis of Ulcerative Endocarditis 

Septic or malignant or ulcerative (they are all used synony- 
mously in clinical medicine) endocarditis is either endocarditis plus 
blood-poisoning, or it is blood-poisoning plus endocarditis, according 
as the valves have been previously or are now only for the first time 
damaged. Its three diagnostic features are: (i) symptoms of 
blood-poisoning; (2) embolic phenomena; (3) valvular bruits — 
and we have to see how it is to be separated from the diseases 
which may at times present these features. 

Simple endocarditis, by which we must here understand one 
from which recovery, except as regards scarring of the valves, is 
easily possible and indeed the rule, has been sketched above, and 
the principal point of difference between it and the malignant form 
is the absence of those extreme variations in temperature, of 
diarrhoea, and of rigors, which indicate that blood-poisoning has 
been superadded to the valvular trouble, though the emboli and 
the murmurs may be common to both. 

To diagnose septic endocarditis from an ordinary case of 
septicaemia, no matter what was the point of entrance of the 
poison, is a work of supererogation ; they are identical. The only 
point is, that the presence of a bruit renders it probable that the 
enemy has effected a lodgment in a position — the cardiac valves — 
whence his spread over the country is supremely easy. If the 
bruit materially and distinctly alters from day to day, we have 
strong proof that active anatomical changes are going on in the 
valve — destruction of tissue or disposition of fibrinous vegetations 
on a raw surface — and these make the diagnosis nearly certain. 

But there are still three specific and special causes of toxaemia 
which are likely to cause confusion. These are typhoid fever, 
acute tuberculosis, and ague. 

Typhoid fever, in its pyrexia and in its diarrhoea, may resemble, 
and is, a septic disease; per contra, a person with old valvular 



iv DISEASES OF THORACIC ORGANS 145 

trouble is not thereby protected from enteric, and in such a person 
the likeness to septic endocarditis may be very close. The following 
differences will, however, usually help us : (a) the fever in typhoid 
is usually more regularly persistent, not so intermittent or remittent 
in its type ; (b) the abdominal tenderness, the headache, and the 
rash are none of them common in ulcerative endocarditis ; and 
lastly, (c) the serum (Weidal's test) test for typhoid will, with almost 
mathematical precision, tell us whether typhoid is or is not present ; 
moreover, (d) if a bruit is present in a patient with typhoid alone, it 
will not alter from day to day in any marked degree. With refer- 
ence to this last point, I must add that, in my view of the pathology 
of septic endocarditis, it would certainly be possible for typhoid to 
relight ulcerative changes in the valves. 

The diagnosis from acute tuberculosis must mainly rest on the 
positive evidence of this disease being present — a preponderance 
of pulmonary signs and symptoms, proof of other tubercular lesions, 
etc. If a cardiac bruit be present, it must be watched for the 
same indications as when typhoid is suspected. Too often, it 
must be admitted, the diagnosis is only cleared up by post-mortem 
examination. 

Malignant endocarditis has been mistaken for ague only by 
reason of a temporary regularity in the rigors and pyrexial 
extremes. The effects of quinine and a few days' delay have 
never left the matter long in doubt, unless death has too rapidly 
intervened. 

Many cases have now been reported in which, while cardiac 
bruits have been absent during life, autopsy has revealed the 
presence of (septic ?) valvular lesions. Of such cases it can only 
be said that, without the assistance of a combination of septic 
symptoms and embolic phenomena, diagnosis is simply impossible. 
We can only guess at it by an attempted process of exclusion. 

Prognosis in Heart Disease 

This involves two separate lines of thought. First, the imme- 
diate prognosis (a) in a case of acute endocarditis, (b) in a case of 
cardiac failure without evidence of acute inflammatory changes; 
secondly, the general prognosis of a case of chronic cardiac trouble 
as regards occupation, etc. 

In a given case of acute endocarditis the prognosis depends 
entirely upon the severity of the inflammatory process, and the 
extent to which it weakens the muscle by its spread. The deter- 

L 



146 DIFFERENTIAL DIAGNOSIS chap. 

mination of this is entirely beyond our powers of direct observa- 
tion ; we can only indirectly estimate it to some degree by the 
symptoms of cardiac failure, and prognosis can only be made from 
day to day by noting each day's progress. When the temperature 
(rarely much raised) becomes quite normal we have a right to 
assume that the active stages of inflammation are at least not pro- 
gressing, and then intensification or amelioration of back pressure 
symptoms gives us a daily despair or hope, always with a tendency 
to look on the bright side, because, as- a matter of clinical experi- 
ence, it is but rarely that acute — provided that it is not septic — 
endocarditis kills directly. Recovery is the rule, at least to the 
extent of a capability of leading a life which may be useful, and 
even enjoyable. When, as in repeated attacks of acute rheumatism, 
we have reason to believe that fresh outbursts of inflammation 
keep on recurring, the outlook must necessarily become more 
gloomy with each attack, though even here we may, to a large 
extent, accept the above suggestions. 

In considering those cases in which we do not suspect recent 
endocarditis, whether the primary trouble has originally been valvu- 
litis or is now essentially a primary muscular degeneration, the 
most important question is, What is it that has caused this heart to 
fail now ; is it that the work has been too great or the power too 
small ? — for evidently the ratio between them is one which cannot be 
maintained. Careful inquiry must be made into the duration and 
progress of each symptom, however trivial, and into the habits and 
surroundings of the patient ; and the less obvious appears the 
excess of work — we must never forget that worry or anxiety, mental 
work, in fact, may be equally or more detrimental than bodily 
exertion — the more anxious are we lest it be power that is failing 
below a standard compatible with prolonged life. When we have 
duly weighed the items of this consideration, we can only await 
next the verdict of treatment. Statistics of bruits, with ages at 
death, are but of little use. As age or degeneration, i.e. loss of 
vital elasticity, advances we must naturally expect a slower response 
to remedial measures, if, indeed, response be not entirely absent ; 
but even now it is astonishing to see how cases may improve by a 
judicious combination and alternation of drugs and of rest and in- 
creasing exertion. The latter, though an obvious common-sense 
method of treatment, has recently been brought into fashionable 
prominence under the name of Schott or Nauheim treatment. 

The prognosis of other cardiac affections, though requiring 
frequently the nicest of judgment, can generally be regarded with 



iv DISEASES OF THORACIC ORGANS 147 

lenient eyes. In nervous affections, as a group, the outlook is 
certainly good, and the patient must be encouraged to live an 
ordinary life, with a few hints as to the avoidance of excesses of 
mental or bodily strain ; and if a cause, such as tobacco or alcohol, 
can be discovered, moderation or total prohibition must be en- 
forced. Even when associated with other phenomena of Grave's 
disease, a rapid heart is comparatively harmless, though a prolonged 
period of ill-health must be accepted as inevitable. 

When "our advice is asked by a patient who has recognised 
valvular disease, with no present symptoms of failure, we must look, 
and encourage the patient to look, on the cheerful side as much as 
possible. Nothing can be more injudicious in such cases than to 
pull a long face and condemn such a patient to a life of idleness, 
ticketed with a label, " Heart Disease." Habits of depressing intro- 
spection are sure to arise, and it is these that kill more surely and 
rapidly than any valvular lesion. Pregnancy is a serious considera- 
tion, but I have known a girl of seventeen with severe mitral trouble 
of rheumatic origin marry at twenty, bear eight healthy children, 
and survive till the age of seventy-seven. In questions where a 
possible pregnancy has to be considered, I think a past history of 
back pressure symptoms of more importance than the present 
character of a bruit. 



CHAPTER V 

DIFFERENTIAL DIAGNOSIS OF SOME SYMPTOMS AND AFFECTIONS OF 
NOSE, THROAT, AND ALIMENTARY TRACT AND ANNEXA 

HEMORRHAGE 

Haemorrhage may appear at the nose, mouth, or anus as the three 
natural openings of the system ; but it may originate from many 
situations, and we shall try to indicate the reasons which lead us to 
assign to it its actual seat of origin. 

Epistaxis, or Bleeding from the Nose 

The nose differs very materially from the mouth and anus from 
our present point of view, because there is practically no difficulty 
in ascertaining that the blood does come from somewhere in the 
naso-pharyngeal cavity itself. When blood makes its exit from 
either of the other two openings the question of precise origin is 
very much more intricate, as we shall presently see. Only as the 
very rarest of clinico-pathological curiosities could one imagine a 
gastric or pulmonary haemorrhage giving rise to more than a pass- 
ing suspicion that the naso-pharynx was its seat, and very little 
inquiry into the mode of onset, and physical examination of the 
cavities, will be required to rapidly settle that suspicion should it 
have momentarily arisen. Consequently, in a case of epistaxis of 
some duration and amount, the only primary questions of diagnosis 
that can arise are (i) its precise seat, and (2) its cause. 

The determination of question (1), though often difficult, or 
even impossible, is, if it be necessary at all, entirely a matter of 
local inspection with mirror and speculum, and will not be further 



chap, v SOME SYMPTOMS AND AFFECTIONS 



149 



considered. The answer to question (2) is a matter of the very 
widest clinical importance, and we will proceed to classify the — 



:. Local Causes : in 
Nose, etc. — 

(a) Traumatism, 

fractured base 
of skull, blows, 
etc. 

(b) Adenoids. 



(c ) Malignant 
growth or in- 
nocent polypi. 
Ulcers, lupus, 
syphilis, etc., 
and necrosis. 

(e) Diphtheria and 
similar acute 
local trouble, 
or even simple 
catarrh. 



(d) 



2. General Constitu- 
tional Causes — 

(a) Haemophilia. 



(b) L e u c o c y- 

thasmia. 

(c) Vascular de- 

generation. 

(d) Onset of acute 

fevers. 

(e) Scurvy. 
{/) Purpura. 
(g) Puberty. 



Causes of Epistaxis 

Diagnostic Points. 

History usually obvious ; difficulties only arise 
when patient is drunk, or otherwise non com- 
pos mentis or unconscious. 

Subject a young child ; suspected by nasal voice, 
sunken bridge of nose, habit of mouth breath- 
ing ; proved by inspection with finger and 
mirror. 

Subject adult probably ; may be complaint of 
local pain, and of nose being stuffed ; inspec- 
tion clears up the case. 

Detected by speculum ; very probably associ- 
ated with ozaena. 



History of illness preceding the epistaxis, 
probably other local signs, swelling, etc. 



and 



Invariably (in first attack) a young subject, most 
likely a boy ; history of previous attacks of 
haemorrhage markedly disproportionate to the 
lesion, e.g. tooth extraction, etc. ; family his- 
tory sure to give evidence of heredity. 

Probably a young subject ; examination of spleen 
and blood will clear up the case. 

Subject old (physiologically, if not in years) ; 
radials thickened, heart hypertrophied ; pos- 
sibly also renal symptoms. 

Subject young ; obviously out of health ; ther- 
mometer proves pyrexia. 

Swollen and spongy gums. 

Always (if epistaxis) purpuric spots elsewhere. 

Age the most important guide, coupled with the 
knowledge that epistaxis does occur frequently 
at this epoch without other obvious causation. 



I S° 



DIFFERENTIAL DIAGNOSIS 



2. General Constitu- Diagnostic Points. 

tional causes — fa 

(/i) Vicarious men- Obviously a female, and with a history of sup- 
struation (?). pressed natural menstruation, but the occur- 

rence of well-established cases is very doubtful ; 
the bleeding would be periodical. 

These causes, as well as those which follow, emphasise the 
absolute necessity of a careful systematic examination of a patient 
with epistaxis if the diagnosis is not at once obvious. 

3. Local Conditions 

other than Nasal — 



(a) Distinct kidney 
disease. 



(b) Cirrhosis of 

liver. 

(c) Morbus cordis. 

(d) Pregnancy. 

(e) Coughing, 

sneezing, etc., 
to excess. 



Diagnostic Points. 

This is only a slightly special branch of 2 (c) 
in which the kidney trouble is, and has been, 
a prominent feature in the case. It is not 
absolutely essential that contracted kidney 
should be present. A consecutive nephritis 
{g.v.) will sometimes cause it. 

History or other strong indication of alcoholic 
excesses ; liver probably enlarged. 

Bruits present, or at least other evidence of car- 
diac disease. 

An occasional cause of epistaxis. History and 
abdominal examination sufficient. 

History distinctive ; onset after such excessive 
respiratory movements. 



Differential Diagnosis of Blood issuing by the Mouth 



Blood which issues by the 
sources : — 



mouth may have obviously many 



1. Naso-pharynx. 

2. Mouth and pharynx. 

3. Stomach or oesophagus. 

4. Lungs. 

5. Aneurysms bursting into either viscus. 

The history of the way in which the blood comes up for evacua- 
tion may in some cases be sufficient and diagnostic, but even in 
intelligent adults the question of vomiting v. coughing is often very 
difficult to settle, so that the differential diagnosis must proceed on 
definite exclusion lines by objective guides as far as possible. 



SOME SYMPTOMS AND AFFECTIONS 



!5! 



Our first care, then, must be, in a doubtful case, to carefully wipe 
away the blood from nose and mouth and fauces ; a careful local 
examination, with thorough exploration with eye or finger, will then 
soon show us whether the blood is coming from above, and reference 
to the causes of epistaxis will probably clear the matter up after a 
systematic examination of the patient. 

N.B. — Do not be led away from a careful examination of nose 
and throat by a definite history of haematemesis (q.v.) or haemo- 
ptysis {q.v.\ especially if other symptoms pointing to stomach or 
lungs are absent. 

Suppose, now, that local examination reveals the mouth or fauces 
as the seat of the bleeding vessel — the following conditions must 
be borne in mind as further elements in the exact diagnosis : — 

Causes of Hemorrhage from Mouth and Fauces 



Diagnostic Points. 



Traumatism from 
external vio- 
lence. 

Traumatism from 
teeth or food. 



3. Gums. 



4. Ulcers. 



5. Acute tonsillitis 

and pharyngitis. 

6. Chronic pharyn- 

geal conditions. 



History obvious. 



Wound found on gums, tongue, cheek, or fauces ; 
its history must be most carefully inquired into, 
whether consciously done by the teeth or dur- 
ing a meal, or attack of coughing, or whether 
the patient is unconscious of its origin. 

A bitten tongue with no history, and with blood 
on the pillow in the morning, in a youngish 
subject is prima facie strong presumptive evi- 
dence of nocturnal epilepsy. 

Spongy, from scurvy or purpura or anaemia, all 
of which will show definite features elsewhere. 
Gingivitis in dentition, or from want of cleanli- 
ness in mouth, easily recognised by age, or by 
tartar encrustation. 

All fairly easily recognised — malignant, syphilitic, 
lupus, tubercle, or simple or gangrenous (can- 
crum oris). 

Easily recognised by dark purplish red coloura- 
tion, or by actual ulceration. 

Blood only in spots ; dilated and varicose veins 
seen on posterior pharyngeal wall. 



As sources of haemorrhage of a serious degree none of these 



52 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



require much consideration beyond mention of the fact that any 
deep or progressive ulceration may open a large vessel ; but as 
sources of alarm to a patient they have a very great and real im- 
portance, and a discovery of one of them may go a long way in 
establishing a reputation for care or carelessness. 

Leaving the mouth and parts open to inspection, we have now 
to consider those seats of a haemorrhage appearing through the 
mouth, which are out of sight. These are — 

i. The air passages, 

2. The alimentary tract, 
and our first point in diagnosis is to determine which of these two 
main tracts is at fault, in other words, to distinguish — 



Sensation accompany- 
ing the voidance of 
the blood. 

Precedent condition of 
patient. 

Associated condition 
of patient 



Voided blood itself. 



HAEMOPTYSIS 

Cough or tickling in 
throat, or possibly 
no warning at all. 

Cough or known lung 
mischief. 

If pallor present, it 
came on subse- 
quently to the hae- 
morrhage, i.e. the 
bleeding excites 
cough before it is 
sufficient to cause 
pallor. 

Usually frothy, and 
often bright (mix- 
ture c air), always 
alkaline. 

Melaena not marked 
as a rule ; some phy- 
sical signs, rales, 
etc., possibly found 
in lungs. N.B. — 
Their absence 
does not exclude 
haemoptysis. 



HjEMATEMESIS 

Nausea first, followed 
by act of vomiting 

Dyspepsia or marked 
gastric disturbance. 

Pallor often precedes 
the ejection of blood, 
i.e. blood pouring 
into stomach causes 
it before the blood 
is voided. 



Never frothy, usually 
dark, and frequently 
acid from admixture 
of gastric juice. 
Associated pheno- Melaena not marked Almost certainly fol- 

mena. as a rule ; some phy- lowed by melaena ; 

possiblylocal pain or 
tenderness over ab- 
domen or stomach. 
Caution — muscles 
may be tender from 
coughing or strain- 
ing. 

Having satisfied ourselves that it is (i) the lung which is the 
source of the blood, diagnosis must next proceed to the— 



SOME SYMPTOMS AND AFFECTIONS 



153 



Causes of Haemoptysis 

Diagnostic Points. 

If within reach of the laryngoscopic mirror, cause 
soon cleared up (tubercular, syphilitic, or malig- 
nant ulceration, q.v., all of them common causes 
of slight haemoptysis) ; blood either in little 
pellets or thin streaks ; sputum very sticky and 
frothy; pain locally on swallowing or coughing. 

Sputum usually uniformly stained either slightly 
or up to prune -juice colour, very sticky and 
usually nearly or quite airless ; associated dul- 
ness, tubular breathing, and temperature, etc., 
commonly distinctive enough. 

Far and away the commonest cause of profuse 
haemoptysis ; bacilli if found distinctive, but 
diagnosis in early stages often impossible. 

All rare causes of haemorrhage ; associated foetid 
smell of sputum, and local physical signs char- 
acteristic. 

Condition described by Sir Andrew Clark: haemor- 
rhage fairly free, physical signs of bronchitis 
and emphysema, without any distinctive bacilli 
or evidence of excavation or dilated tubes. 

History usually sufficient of choking with aspira- 
tion of the foreign body. 

As a cause of haemoptysis rare, but when aneurysm 
is present haemoptysis is tolerably frequent ; if 
other signs of aneurysm present, haemoptysis 
adds to their weight, and especially if there are 
signs of pressure on a large air tube. N.B. — 
Slight haemoptysis may precede for a long 
period the actual rupture of the sac. 

Said to be like red-currant jelly, but in my ex- 
perience the haemorrhage here is only dis- 
tinguishable by the physical signs of the growth, 
and has nothing distinctive in itself. 

Vide tests between haematemesis and haemoptysis ; 
if definite haematemesis proved to be present 
there will only be slight pellets of blood or 
blood-stained mucus coughed up for a few 
hours or a day or so after the vomiting. 

These causes really fall into two clinical groups, viz. those in 
which the source and cause of the haemorrhage are obvious or 



Laryngitis, trache- 
ites, bronchitis 
acute, and granu- 
lar pharyngitis. 



Pneumonia. 



Phthisis. 

Gangrene, abscess 
bronchiectasis. 

Degenerative bron- 
chitis and em- 
physema. 

Foreign body. 

Aneurysm. 



Malignant growths. 



Blood aspirated into 
lung in haemate- 
mesis. 



54 



DIFFERENTIAL DIAGNOSIS 



easily detected, and those in which probabilities have to be nicely 
balanced. To the former group belong visible laryngeal and pharyn- 
geal troubles, obvious gangrene, abscess, aneurysm, pneumonia, 
and carcinoma secondary to an obvious primary growth. To the 
latter belong those cases of definite haemoptysis in which no physical 
signs at all are to be found, and those in which the physical signs 
are those of bronchitis plus a few rales and fine crepitations, indicating 
the present situation of the semi-coagulated blood ; in this group 
our main anxiety is the determination whether phthisis is at the 
bottom of the matter or not, and the question will be found dis- 
cussed under that heading {vide pp. 54 and 92). 

We will now assume that (2) the blood has come from some part 
of the alimentary system. We have to consider the — 

Causes of H^ematemesis 



Swallowed blood 
(rarely of notice- 
able extent). 

Vicarious menstrua- 
tion (very rare). 

Bloodstates in — 
Purpura, 
Scurvy, 
Yellow fever, 
Acute yellow 
atrophy of 
liver, etc., 
Traumatism. 



Gastritis or simple 
vomiting. 



Diagnostic Points. 

Already considered ; local examination usually 
sufficient to clear up the case, except in a few 
cases of malingering, with deliberate drinking 
of blood. 

Of very doubtful occurrence; can only be thought 
of in a girl, probably young and hysterical ; no 
other local symptoms, periodicity of bleeding. 



All rare as causes of 
haematemesis. 



Aneurysm. 



The condition of the 
patient induced by 
the named disease 
usually quite suffi- 
cient for diagnosis. 

History sufficiently obvious, either of an external 
blow or of swallowing a corrosive or violent 
irritant, or some mechanical lacerator of 
mucous membrane. 

Haemorrhage slight as a rule, and usually only 
in streaks ; the history of severe vomiting pre- 
ceding the blood usually sufficient, except in 
those cases where the violence has actually 
ruptured a large vessel ; vide below, Aneurysm 
and Ulcer, etc. 

Quite possibly unrecognised till post-mortem is 
made ; only diagnosable during life when 



SOME SYMPTOMS AND AFFECTIONS 



55 



Cancer. 



Ulcer. 



Diseases of other 
organs leading to 
venous conges- 
tion — 

(a) Morbus cordis. 

(b) Chronic pulmon- 

ary disease. 

(c) Cirrhosis of liver. 

(d) Portal conges- 

tion. 



Diagnostic Poii 
previous examination has revealed a tumour of 
abdomen with expansile pulsation. Haemor- 
rhage very profuse, and probably rapidly fatal. 

Haemorrhage usually of coffee ground type, great 
loss of flesh, and probably a tumour ; patient 
usually beyond early middle age. 

Haemorrhage usually free, with clots ; in simple 
ulcer, patient usually a young person and 
more commonly a female. I have known a 
tubercular ulcer in a phthisical patient cause 
fatal haemorrhage, but such cases are very rare. 



Presence of bruits and other evidence of cardiac 

back pressure. 
Evident physical signs of lung disease, associated 

with failure of circulation. 
History of alcohol, or dyspepsia and vomiting 

suggestive of alcohol ; liver enlarged probably. 
Produced by ascites, carcinoma of peritoneum, 

enlargement or diseases of spleen, etc., with 

tolerably obvious features. 

Such is a practically complete list of the causes of the presence 
of blood in the stomach leading to haematemesis. In numbers 
they look formidable enough on paper, but in practice they are 
comparatively simple in diagnosis. Thus, haemorrhage from the 
stomach is never the first and totally unexpected symptom of serious 
bloodstates, nor of those forms of back venous pressure commonly 
attributed to portal congestion. There are and have been some 
prodromal or leading indications in all cases, the haematemesis 
forming a culminating calamity, so to speak, not perhaps expected, 
but not altogether unforeseen. There is only one group of cases 
that really presents much difficulty, viz. those in the middle period 
of life, especially in men, where we have to try and decide between 
cirrhosis of the liver, carcinomatous or simple ulceration, and an 
unexplained cause which provisionally may be termed simple 
varicosity of veins. More than one such case has occurred to me 
in which age and sex, history of alcohol, slight dyspeptic pheno- 
mena, and the entire absence of positive objective signs (enlarged 
liver, tumour, dilated stomach, etc.), have together formed a 



156 DIFFERENTIAL DIAGNOSIS chap. 

symptom-complex, in which the diagnostic points have been so 
nicely balanced that a positive diagnosis has been impossible in the 
absence of a post-mortem. Luckily for the patient the diagnosis, 
from a therapeutical point of view, is here of comparatively little 
moment, for absolute rest in bed, combined with physiological rest 
for the stomach, constitute the main, if not the only means of com- 
bating all form of serious gastric haemorrhage. For some further 
indications, vide under the headings of Ulcer, Cirrhosis of Liver, etc. 

Anal Appearance of Blood 
We must now consider blood passing from the bowel by the 
anus. It may be laid down as a working rule that blood in a 
comparatively unaltered state, i.e. recognisable as such by the laity, 
passed per anum comes from the colon or rectum, or the lowest 
two feet or so of the ileum. Blood coming from the stomach or 
upper part of the small intestine will be so altered by the digestive 
processes as to appear as melaena or black tarry stools. The only 
exception (it occurred to me once in tubercular ulcer of the 
stomach, verified post-mortem) is a case in which the bleeding is so 
profuse as to practically fill the intestine, and so appear at the anus 
simply darkened in colour. Such cases are almost invariably fatal. 

The following are the Causes of Melaena 

Blood passing from These cases constitute an enormous majority 
the stomach. (probably 90 per cent) of cases of melaena ; 

haematemesis is very likely to have occurred ; 
for differential diagnosis, vide table above. 
Duodenal ulcer, or Rare as causes of melaena ; suggested chiefly by 
simple, tubercular, the presence of the symptom (melaena) com- 

or malignant dis- bined with the absence of the commoner 

ease of small in- causes ; possibly some tumour felt or some 

testines. abdominal symptoms suggesting ulceration, 

but not of a gastric type. 
Ankylostomiasis. Very rare indeed in England as a cause of 

melaena and anaemia ; only to be detected by 
finding eggs in the faeces. 

Causes of Hemorrhage (recognisable as such by the Laity) 
passing per Anum 

A. Lower ileum — Diagnostic Points. 

Ulcers : Typhoid. Haemorrhage appearing in course of a definite 
attack or of a vague pyrexial illness, when the 
haemorrhage clears up the diagnosis. 



SOME SYMPTOMS AND AFFECTIONS 



iS7 



Tubercular. 



Dysenteric. 
Simple and car- 
cinomatous. 



Traumatism. 



Drugs, especially 

violent purges. 

Blood conditions. 



Intussusception. 

B. Caecum, colon, 
and sigmoid 
flexure. 



Diagnostic Points. 

Usually distinct indications of tubercle, but 
diagnosis often impossible, ante mortem, from 
typhoid ; vide Typhoid v. Tuberculosis. 

History of recent or old dysentery fairly obvious. 

To me unknown causes of severe haemorrhage, 
but might conceivably give rise to the symptom, 
but would not be diagnosable, except by ab- 
sence of above three troubles, and in carci- 
noma possibly a tumour. 

History of a blow or swallowing a foreign body. 
If such a case arose it would be quite a patho- 
logical curiosity. 

History of administration. 

The same as in the stomach, but all rarer ; occa- 
sionally has occurred as a sequel to the very 
debilitating scourge of influenza ; such was the 
cause of death of a lately deceased distin- 
guished member of our profession. 

Signs of intestinal obstruction, presence of strain- 
ing, etc. 

All similar causes to those of ileum, but dysen- 
teric and carcinomatous ulceration are here 
very common causes of haemorrhage instead of 
being rare, while the reverse is the case with 
typhoid and tubercular troubles, intussuscep- 
tion commencing in colon very rare indeed. 



C. Rectum — 
Traumatism. 
Piles. 
Polypi. 
Prolapse. 

Intussusception coming down. 
Ulcers — dysenteric, malignant, 

etc. 
Strictures. 

Fissures, fistulae, etc. 
Vaginal sources, to be looked 

for in females. 



All within reach of the examining 
finger or speculum, so that their 
diagnosis requires no discussion ; 
examination of the rectum also 
discloses the fact that the blood 
does come from the lowest six 
inches of the bowel. 



Like haemorrhage appearing by the mouth, the causes of 
melaena and rectal haemorrhage are much more formidable on 



158 DIFFERENTIAL DIAGNOSIS chap. 

paper than in practice, and it is but very rarely that some clinical 
features will not be found leading unmistakably to a definite 
diagnosis. 



VOMITING 

Vomiting is a very complex process, of which the actual 
emptying of the stomach forms only a culminating objective 
feature. According to physiology, the whole series of phenomena 
ending in emesis is best explained by the hypothesis that there is 
situated in the medulla oblongata a group of neuron cells (termed 
a vomiting centre), the dendrites of which are connected with the 
nervous system in such a way that, on the one hand, they may 
receive afferent impulses from any part of the body, which im- 
pulses are capable of stimulating them to special activity, and, on 
the other, they may transmit messages to the salivary glands, to 
the respiratory mechanism, and to the voluntary muscles which, 
when thus stimulated, produce the emptying of the gastric contents. 
By accepting this explanatory hypothesis, we are in a position to 
gain a more or less rational understanding of the innumerable 
pathological or clinical incidents that may be associated with 
vomiting. The afferent impulses (as from a crush or severe pain, 
however excited) from any part may be so strong as to cause it, 
or, on the other hand, the condition of the blood circulating 
through the centre, or the physical condition of the brain, may be 
such as to independently start the centre into action. Lastly, and 
far most frequently, the contents or condition of the stomach 
itself may start the afferent impulses. 

A purely scientific or physiological analysis of vomiting should 
therefore start with a division into central or direct, and peripheral or 
reflex, each with its subdivisions; but from a clinical and diagnostic 
point of view a more useful classification is into the following : — 



SOME SYMPTOMS AND AFFECTIONS 



59 



Causes of Vomiting 



Diagnostic Indications 



("Cerebral — 
Tumour. 
Meningitis. 
Cerebritis, etc. 
General shock. 



Gastric crises of 
tabes dorsalis, or 
G.P.I. 



Hysterical. 



Cardiac disease. 

Pulmonary diseases 
attended by 
cough — phthisis, 
etc. 



Acute infective dis- 
eases — the zymo- 
tics, pneumonia, 
etc. 

Uraemia and other 
kidney troubles. 



Simple pain. 



Not usually associated with much nausea, 
independent of food ; almost invariably as- 
sociated with marked corroborative evi- 
dence — optic neuritis, fits, paralysis, etc. — 
may be quite intermittent for even long 
periods, and then its apparent causeless- 
ness is its great feature. 

Apparently quite causeless in its onset, and 
equally mysterious in its cessation after a 
day or two's duration : also independent of 
food, associated with more local pain than 
cerebral form. 

Probably in a young person, and one who is 
not losing flesh, notwithstanding the asser- 
tion that for months everything has been 
vomited. 

Distinct evidence of bruits and back pressure 
on other organs than the stomach. 

On inquiry patient will say, " I cough till I 
am sick." Physical examination rarely 
fails to show good cause for the cough, but 
it is astonishing how patients will complain 
of the vomiting and forget the cough till a 
leading question on it is put: "Are you 
sick because you cough, or are you sick 
independently of coughing ? " 

Although vomiting, especially in children, is 
common at the onset of febrile acute 
illnesses, it must be very rarely that the 
cause is not soon obvious, for the ther- 
mometer will rapidly remove doubt. 

Vomiting again causeless, and independent of 
food ; uiinary examination soon clears up 
the case, even if it be unattended with 
commoner symptoms of uraemia. 

Statement made by patient quite sufficient. 



a 


Gastric trouble — 


o 

V 


Ulcers. 


u 

o 


Irritation. 


ID 


Inflammation. 


rt 


Pyloric obstruc- 


n 


tion, etc. etc. 


Q 


^ Poisoning. 



1 60 DIFFERENTIAL DIAGNOSIS chap. 

Pregnancy, tumour, Physical examination of the abdomen very 
obstruction, etc. soon clears the matter up ; abdominal 

pain or discomfort usually marked. 

Addison's disease. Vomiting usually associated with pain, but 
the accompanying physical weakness, and 
especially the almost imperceptible pulse, 
will point to the disease even if typical 
bronzing be not present. 
Vomiting due to actual disease of the 
stomach is, broadly speaking, characterised 
by being in some definite relationship to 
food and to pain or discomfort produced 
by food. 

For other points separating the various 
gastric troubles, vide Gastric Ulcer, etc. 

If we are called upon to investigate a case of vomiting, very 
little observation is required to eliminate certain of the above 
groups — the pyrexia and aspect of acute general diseases, the 
collapsed features or the history of obstruction, the evident dropsy 
of morbus cordis, the pain or shock of an accident, etc., will at 
once put even the most careless observer on the right track. The 
diagnostic difficulties begin when the vomiting is the sole obvious 
feature that attracts the anxious attention of the patient or of the 
friends in the case of children. 

In quite young babies, i.e. in the first year of life, it is almost 
safe to conclude at once that food and consequently gastric irrita- 
tion, is at the bottom of the mischief, though we must not forget to 
look for signs of congenital syphilis. After the first year up to, say, 
puberty the insidious onset of tubercular meningitis with causeless 
vomiting must never be absent from our minds, however obvious 
may seem at first sight the apparent cause for the symptom. It is 
also during this period of childhood that all acute illnesses are apt 
to have vomiting for a prominent feature in their early stages, from 
which fact we may safely deduce as a golden rule — No case of 
vomiting in a child can be safely despised till a few days have passed 
without the development of any more guiding symptoms. It may, how- 
ever, be said that in acute gastric conditions food will be at once 
rejected, while in all other forms of sickness the food will usually 
stay down for some little time, and that without pain or discomfort. 

In adults we maydraw attention specially to " morning vomiting " ; 
this, when repeated, is almost confined to the following conditions : 
pregnancy, alcohol and alcoholic dyspepsia; occasionally the vomiting 



v SOME SYMPTOMS AND AFFECTIONS 161 

of uraemia and of cerebral tumour assumes this type, as almost 
invariably does the vomiting which is brought on by the cough 
of chronic bronchitis. Once reminded of this peculiarity diagnosis 
is not difficult. 

COLIC 

Strictly speaking, the terms " colic " and " colicky pain " should be 
reserved for intermittent or at least remittent painful sensations in 
the abdomen, or referred to the abdominal viscera ; but I wish here, 
for convenience' sake, to use the expression in a more comprehen- 
sive sense to include all forms of severe pain referred by the patient 
(either by voice, or gesture in those unable to speak) to the ab- 
dominal or pelvic region. Pain thus referred may arise from 
disease of any structures of the trunk below the thorax, for none of 
the viscera were intended for organs of special localising sense, 
so that pain arising in one part is frequently misreferred to another 
spot. For this very reason the differential diagnosis of the various 
causes for the symptom assumes here a greater importance than 
in any other region, especially as the treatment for one cause 
of the pain would be absolutely and rapidly fatal if another cause 
were at work, e.g. perforation of stomach v. a gall-stone. 

The causes, then, are many and various. They may be divided 
most simply into groups : — 



CAUSES OF ABDOMINAL PAIN 

Group I. — Affections of the Peritoneum and Alimentary Canal itself 

(a) Irritating contents of the gut causing either congestion of 
mucous membrane or painful peristalsis, or more likely 
both together. 
Food unsuitable in quantity or quality. 
Foreign bodies of any description. 
Drugs, active purgatives, or poisons. 
(a) Ulceration and other disease of the walls ; simple ulcer or 
tubercle, or carcinoma, etc. {N.B. — It is astounding how 
frequently such diseases exist without causing any pain 
directly by their mere presence.) 
(c) Embolus of a mesenteric artery I have known to cause 
intense agonising colic with other symptoms like obstruc- 
tion. 



1 62 DIFFERENTIAL DIAGNOSIS chap. 

(d) Obstruction and strangulation of the gut, whether acute or 

chronic, and however arising (intussusception bands, 
hernia, twists, etc.). 

(e) Peritonitis, acute or chronic, local or general, however aris- 

ing, independently or through — 
(/) Perforation of any hollow viscus, or rupture of a solid one. 
(g) Some blood alterations or blood-carried poisons must be 

inserted here ; of these lead and gout are the only two 

of practical importance. 
(/;) Nervous disturbance of gut from independent disease or 

functional condition of cord or brain ; e.g. the gastric 

crisis of tabes, or of G.P.I. ; or disease of the supra- 

renals ; or abdominal nerve complexus as met with in 

Addison's disease, etc. 



Group II. — Affections of Organs in Direct Connection with the Gut 

(a) Liver : — 

Inflammation or abscess, primary or arising in connection 
with a previous painless affection. 

Carcinoma and other rapidly increasing growths. 

Gall-stones when trying to leave the gall-bladder. 

Rupture (only traumatic). 
(6) Pancreas : — 

Acute inflammation. 

Stone in the duct (very rare, and practically outside the 
range of certain diagnosis). 

(c) Spleen : — 

Abscess. 

Enlargement, especially if also mobile enough for difficulties 

to occur in the circulation to and from it. 
Embolus (pain rarely very severe). 

Group III. — Affections independent of the Alimentary Tract and its 
Cofinections 

(a) Of the urinary tract : — 

Stone or other painful kidney trouble. 
Kinking or disease of ureter. 
Bladder : distension or rupture. 

(d) Abscess from any source ; its presence or its rupture may 

cause acute pain. 



SOME SYMPTOMS AND AFFECTIONS 163 

(c) Aneurysm : its presence or rupture. 

{d) Affections of the bones of the vertebral column, especially 



Group IV. — In women the pelvic reproductive organ must be 
borne in mind as the possible primary source of growths, 
abscesses, peritonitis, bladder disturbance, etc. 

In dealing practically with such a heterogeneous collection of 
causes for acute abdominal pain, it is obvious that we must have 
some guiding principle on which to work ; though a general, and 
often even a precise and exact, diagnosis is by no means so difficult 
to arrive at as might at first sight appear. The simplest method 
appears to me to take events in the chronological order in which 
they occur, with possible or probable narrowing of the field with 
each. On a message being received to see a patient in this condi- 
tion, the first information naturally given is, roughly, the age of the 
patient, baby, child, or adult. We may say at once that in subjects 
under puberty direct alimentary disturbances are almost alone 
to be thought of — intestinal obstruction or strangulation, simple 
colic, possibly appendicular trouble or peritonitis, or may be even a 
renal stone — but such cases as tabetic crisis, Addison's disease, 
aneurysm, gall-stone, etc., may be at once excluded. After puberty 
no such general rule can be laid down, though it is true that certain 
troubles, e.g. gall-stone and malignant obstruction, are much more 
frequent in stout elderly patients than are others, e.g. intussuscep- 
tion or perforating acute ulcer. 

The next step, as things occur in practice, is to inquire of the 
friends as to the previous illnesses of, or similar attacks experienced 
by, the patient, and also as to symptoms additional to the pain : — 

Is this the first attack ? 

A. If not, has the patient previously — 

Been jaundiced ? 

Passed gravel ? 

Had urinary trouble or difficulty ? 

Complained of anything suggestive of G.P.I, or tabes ? 

Suffered from marked irregularity of bowels ? 

Lost much flesh, or rapidly emaciated ? 

B. If it is, How did it come on ? Was it — 

(a) More or less gradually in the course of a fairly definite 



1 64 DIFFERENTIAL DIAGNOSIS chap. 

illness, or at least has the patient been complaining 

long? 

e.g. Typhoid. Gall-stones. 

Addison's disease. Gastric ulcer. Dyspepsia. 

Phthisis. 

Gout. 

or, {&) Suddenly, in the midst of perfect health ? 
e.g. Latent gastric ulcer with perforation. 
Hernia or other strangulation of gut. 
Appendicular trouble. 
Indigestible meat, poisons, etc. 

The answers to these questions, and independent statements by 
friends, will very probably have thrown great light upon the case, 
excluding certain causes almost to a certainty, and biinging others 
forward into equal prominence as probabilities. Any symptoms 
additional to the pain will also very likely throw great light in 
certain diagnostic directions. Those more particularly to be asked 
for if information is not volunteered are — 

Vomiting. 

Constipation or other state of bowels, such as straining at stool, 

or diarrhoea. 
Strangury, or frequency of micturition, or other obvious urinary 

trouble. 
History of blow, or other accident. 

After gaining as much information as possible from what may 
be called external sources, the next step is to visit the patient and 
make as careful an examination, verbal and physical, as circum- 
stances will permit. 

We will now for a moment leave diagnosis itself, to consider 
the object we have to gain by it, viz. correct treatment of the 
condition. 

Treatment of acute abdominal pain must proceed on one of 
four lines : — 

A. Absolutely expectant, except for the outward application of 

hot fomentations, or an ice bag; 

B. A hypodermic injection of morphia, or inhalation of general 

anaesthetising agents, such as chloroform or ether ; 

C. An emetic or purge ; 

D. Prompt surgical interference : manipulative or by the knife ; 



v SOME SYMPTOMS AND AFFECTIONS 165 

and it is primarily the object of diagnosis to determine upon which 
of these lines we may most safely proceed. 

The last is out of all proportion the most important from every 
point of view, so we will first investigate the symptoms which indi- 
cate that a condition is present which demands this line of treat- 
ment. The conditions themselves are : — 

1. Perforation or rupture of any hollow or solid viscus (gut, 

bladder, uterus, liver, etc.), or of any pathological 
tumour in the widest sense of the word (aneurysm, 
cyst, abscess, etc.). 

2. External strangulation (strangulated hernise of all sorts 

palpable externally), or internal strangulation of a viscus 
or tumour by twist of its pedicel, or by band, etc. 
(internal herniae, etc.). 

3. Acute general peritonitis of unknown origin (as well as 

most cases of known definite causation). 

4. Acute pancreatitis and embolus of a mesenteric artery, 

which cause symptoms precisely resembling those of 
strangulation of the gut, and can only be distinguished 
on operation. 

5. Distended bladder. 

6. Displacements of pregnant or pathological uterus, causing 

urgent symptoms. 

Luckily most of these conditions are, even in their earliest stages, 
usually associated with such diagnostic features as to be at once 
recognisable as a group of cases. Thus the — 

Pain. — Is very sudden in onset, rapidly becoming agonising in 
character, may be continuous or intermittent, and in many 
external hernial cases so correctly localised as to direct 
attention at once to the seat of trouble. 

Aspect of the Patient. — Is frequently distinctive, with ashen pallid 
face, and eyes deeply sunk, and pinched features ; collapse 
very profound, with cold and clammy sweat. 

Pulse. — Is small, thready, and frequent. 

Tongue. — Is very dirty, and with great tendency to dryness. 

Vomiting. — Is often incessant, most distressing, very rarely 
indeed quite absent; if any delay has occurred may be 
stercoraceous. 



1 66 DIFFERENTIAL DIAGNOSIS chap. 

Constipation. — Absolute since the onset of pain ; thus dis- 
tinguishing such cases from virulent poisons, in which 
diarrhoea is present with vomiting. 

Abdo7nen. — Is very tender to touch as well as painful, and may 
be already distended or rapidly becoming so ; evident 
laboured waves of peristalsis may be present and give useful 
information. 

Urine. — May be much diminished, or totally suppressed without 
strangury. 

Should all these indications be present, or even two or three of 
them in well marked form (especially small, thready pulse, dry 
tongue, and incessant vomiting), there can be no room for hesitation 
if life is to be saved — piompt surgical measures must be adopted, 
manipulative or by cutting, according to circumstances. It how- 
ever only too frequently happens that the symptoms are not so 
well marked at the onset, and diagnosis must perforce be postponed 
for an hour or two. The only safe and golden rule is then : " In 
any case presenting the above features in doubtful form, but where 
suspicion is in the slightest degree aroused, no morphia must be 
administered"; for thereby many of the most important developments 
are masked or prevented ; but the patient must be placed under 
intelligent observation with hot or cold abdominal applications, and 
his case must be reinvestigated in an hour or two, by which time 
the diagnosis will have become more certain. Measures may then 
be taken accordingly. 

A distended bladder, though possibly a cause of acute abdominal 
pain, ought not to be difficult of diagnosis ; if the distension is 
sufficient to cause pain, the viscus will always be easy to feel as a 
centrally placed abdominal tumour. A bladder ruptured through 
disease, though probably causing symptoms belonging to (i) 
(where, indeed, it has been placed), will have invariably been pre- 
ceded by a long history of urinary trouble and difficulty, and will 
have thus been diagnosed. 

The pregnant uterus will likewise not offer, under these circum- 
stances, any diagnostic difficulty. Cases of rupture come under 
(i), and the blanched, bloodless aspect of the collapsed patient will 
be suggestive in a woman known or suspected to be pregnant. 

Into the more definite diagnosis of these cases I do not propose 
here to enter : the keenest diagnostician must frequently content 
himself with saying, " Laparotomy is urgently indicated," leaving 
the operation to disclose the exact condition. Thus, acute pancrea- 



v SOME SYMPTOMS AND AFFECTIONS 167 

titis presents all the features of acute intestinal strangulation, and 
acute perforative peritonitis is often identical in its symptoms with 
volvulus or internal hernia. 



Abdominal Cases without Marked Collapse 

Collapse developing very early in the case (almost from the 
instant of onset), with its attendant fades, pulse, etc., we have 
hitherto taken as the guiding principle in diagnosis. We have now 
to consider those cases of abdominal pain in which it is not so 
marked, may be even absent, at any rate in the earlier stages. 
Such cases, especially if on examination no pathognomonic sign 
is present, still call for the keenest eye, clearest understanding, 
and most incessant watchfulness, that at the earliest moment the 
cloven hoof betraying serious developments may be detected — 
something more than pain written in the face, some smallness 
and frequency of pulse out of proportion to the expected; a 
persistency of vomiting, or alteration in the character of the 
vomited matters — any or all of these features may be found on a 
second visit. 

In no case of painful abdominal affection can it be said that 
collapse must be absent, but it is, at any rate in severe shape, an 
exceptional feature in otherwise fairly healthy people (at the ex- 
tremes of life or in broken down subjects great caution in judgment 
is necessary), when one of the following is present, causing complaint 
of abdominal pain : — 

Simple colic, from improper contents of gut, or due to lead, 
gout, or Addison's disease, or nervous troubles ; 

Liver diseases, apart from a possible suppurative peritonitis 
arising from it ; 

Chronic obstruction of bowels ; 

Typhlitis ; 

Aneurysm ; 

Caries of spine ; 

Retroperitoneal growth ; 
and we shall now proceed to discuss their differential diagnosis on 
the assumption that the patient is capable of giving intelligent 
answers to questions, and that a thorough examination of the 
abdomen is allowable and allowed. 

On approaching the patient definite jaundice, if present, will at 
once attract notice {N.B. — by artificial light this is very easily over- 



1 68 DIFFERENTIAL DIAGNOSIS chap. 

looked, in fact, impossible to detect, and the question of its presence 
must always be asked), and direct attention to the liver as in some 
way the cause of the trouble. The discovery of jaundice would 
also lead to questions as to its previous occurrence, if such had not 
already been put. The pigmentation of Addison's disease would 
at this stage possibly attract attention, and if present go far towards 
the elucidation of the diagnostic problem. 

General inquiries to establish points left doubtful by the friends 
may then be put to the patient ; their scope has been already 
indicated. The abdomen must then be exposed, and the patient 
asked to point out the seat of greatest pain, and the direction (if 
any) in which it seems to travel ; this point is often useful, but as 
already noted, too much stress must not be laid upon it, owing to 
the vagaries of referred pain. 

The orderly methodical examination of the abdomen by inspec- 
tion, palpation, and percussion, and even by the stethoscope, may be 
proceeded with, and if there is still a doubt, a vaginal or rectal 
examination, or both if necessary, must be made. 

This examination will almost for a certainty have revealed any 
of the following points which are present : — 

i. Whether the pain is greatly increased by pressure, or some- 
what relieved as a steady pressure becomes firmer and deeper ; the 
former suggestive of peritonitis or serious organic disease, the latter 
of simple colic. 

2. Hardness or increased resistance of the muscles, either locally 
or generally, suggestive of some inflammatory trouble beneath them. 

3. Tumour or swelling of liver, spleen, kidney, or bladder, or 
independently existing in abdomen, suggestive of its being the 
real seat and possible cause of the pain, or indirectly affording an 
opportunity for obstruction or strangulation of the gut. 

4. Per vaginam, fixity, or swelling of uterus, or other palpable 
abnormal condition of female reproductive organs again directly or 
indirectly causing the mischief. 

5. Per rectum, ballooning, or the peculiar smell of carcinoma 
(not easy to describe, but like some other smells once experienced 
never forgotten) or definite stricture, or tumour within reach of 
finger, all suggestive of carcinoma or other serious rectal disease, or 
intussusception reaching the rectum. 

6. In cases still obscure we shall have tried to elicit pain on 
flexing thigh against resistance, suggestive of renal or appendicular 
or psoas mischief, or tenderness on tapping or jarring spine, sug- 
gestive of caries or other serious bone mischief. 



v SOME SYMPTOMS AND AFFECTIONS 169 

Founded upon these and similar features, we may epitomise the 
principal points of differential diagnosis in such cases as follows : — 

Differential Diagnosis of Causes of Abdominal Pain not 
usually associated with marked collapse, or urgently 
demanding active interference 

Colic, Simple or Functional, of Intestine 

Probable history of an over-full, indigestible, or unsuitable meal ; 
pain probably relieved or not made worse by pressure ; vomiting 
severe, but not prolonged, and diarrhoea probably present, or soon 
sets in. 

Lead and gout must be thought of in adults as a possible cause, 
and a blue line on gums or tophi looked for, and inquiries made of 
occupation, etc. 

Tabes dorsalis and G.P.I, must also be remembered in this con- 
nection, and the knee jerks and pupils investigated. 

After all is said and done, the most important problem is here 
to separate these cases from commencing local or general peri- 
tonitis, and from forms of intestinal obstruction which begin in- 
sidiously (overlooking a gall-stone or renal calculus is less serious, 
but vide below), and the vital importance of the subject must be my 
excuse for repeating and bringing into closer contrast the likenesses 
and differences of the two conditions. 

Besides the mere pain itself, then, they may be alike in — 

1. The vague localisation of the pain. 

2. The suddenness of its onset. 

3. The universal tenderness of the abdomen on light pal- 

pation. 

4. The intensity of the pain. 

But they more frequently and essentially differ in — 

Obstruction and Peritonitis. 

Not unfrequently cor- 
rectly localised. 

Most commonly abso- 
lutely sudden, and 
then persistent at a 
high pitch. 

May be great, but is 
never greater than 





Functional colic. 


Locality. 


Very vague, usually epi- 




gastric or umbilical. 


Suddenness. 


Gradually rising to a 




maximum, and waning 




and waxing. 


Superficial tender- 


Often great, in fact, 


ness. 


greater than when 



170 



DIFFERENTIAL DIAGNOSIS 



Collapse, includ- 
ing sunken eyes, 
small pulse, 
dry tongue, 
clammy sweat, 
etc. 

Vomiting:. 



Constipation. 



Diarrhoea. 



Functional Colic. 

fairly firm pressure is 
applied, which may 
completely check the 
pain. 
Rarely present, except at 
extremes of age and 
in broken - down sub- 
jects. 



Rare, except in acute 
poisoning by drugs or 
food, and then never 
stercoraceous,and only 
excited by food. 

Not common, except in 
lead poisoning. 



Far more frequent than 
constipation, except in 
lead colic. 



Abdominal swell- Practically do not occur, 
ing or tympan- at any rate early in the 

ites. case. 



Muscular rigidity. 



Easily overcome, if pre- 
sent, by gentle, steady, 
persistent pressure. 



Obstruction and Peritonitis. 

that caused by firm 
pressure. 



Usually comes on at 
once, and in any case 
develops very rapidly; 
only in the rarest of 
instances is it quite 
absent. 

Very common indeed, 
usually very persist- 
ent, and may be ster- 
coraceous, independ- 
ent of food. 

Usually complete (even 
to wind) after the 
onset of pain ; bowels 
may have been open 
just previously or pain 
may come on during 
defalcation. 

Only exists in the shape 
of tenesmus, with pass- 
ing of mucus and 
blood. N.B. — In sus- 
picious cases, when 
diarrhoea is complained 
of, examine the alleged 
motions. 

General distension fre- 
quent, and forms a 
very suspicious feature 
indeed. May arise 
very early in the case. 

May be quite local, but 
is usually present, and 
cannot be overcome, 
any effort to do so 
causing great increase 
in the pain. 



In the remaining conditions causing severe abdominal pain, 



SOME SYMPTOMS AND AFFECTIONS 



171 



immediate diagnosis on the first or even second visit is of less 
vital consequence, though important enough, as it must essentially 
be, if medicine is to maintain any grounds of claim to rank as a 
science. 



Affections of the Liver 

Simple non-purulent Two cases have recently come under my care in 
inflammation or which I believe this condition was present ; 

congestion. the pain was localised to the right hypochon- 

driac and epigastric region, and both were 
associated with a distinctly appreciable liver 
edge, which was very tender on pressure or 
manipulation ; in both alcohol was much in 
evidence, and both subsided in a few days 
without further symptom. 

Suppuration. Probable history of dysentery or tropical resi- 

dence ; pain localised correctly in liver ; fre- 
quently a swelling to be made out ; a hectic 
type of temperature, and especially if associated 
with night sweating, is very suspicious. 

Carcinoma. Easily diagnosed if tumour is felt ; if no tumour, 

then rapidity of loss of flesh is most important 
feature, when the locality of pain, and age of 
patient, rouse a suspicion. 

Gall-stones. Possibly previous history of jaundice ; patient 

usually stoutish and middle-aged or older ; 
distended gall-bladder, if present, almost con- 
clusive. 



It is usually assumed that gall-stones, renal calculus, and simple 
colic are very likely to be mistaken for one another. The following 
table shows their contrasts and likenesses : — 



Gall-stones, renal calculus, simple colic may be alike in- 



1. Sudden onset of pain. 

2. Sudden cessation of pain. 

3. Indefinite locality of it. 

4. Severity of it. 



172 



DIFFERENTIAL DIAGNOSIS 



They more commonly differ in- 







Gall-stones. 


Renal Calculus. 


Simple Colic. 


5- 


Locality 


Usually referred 


Usually in back, 


Usually referred 




and — 


more correctly 
than the others 
to the right 
hypochon- 
drium. 


loin, and groin. 


to umbilicus or 
epigastrium. 


6. 


Direction 


Pain fixed, or 


Travels down 


Fixed in umbili- 




of pain. 


seems to pass 


groin to testi- 


cus, or travels 






upwards. 


cle, which is 
frequently re- 
tracted. 


across abdo- 
men. 


7- 


Character. 


Not intermittent. 


More intermit- 
tent than gall- 
stone. 


Usually is actu- 
ally intermit- 
tent. 


8. 


Calculus 
found. 


In faeces if at 
all. 


In urine if at all. 


None. 


Associated 


Jaundice ; urine 


Strangury or fre- 


Urination not in- 




symptoms, 


dark coloured 


quent micturi- 


terfered with, 




if any. 


perhaps; other- 


tion ; possibly 


except possi- 






wise the func- 


bloody urine ; 


bly quantity 






tion not inter- 


function pretty 


diminished if 






fered with ; 


certainly inter- 


much vomit- 






vomiting may 


fered with; 


ing, which is 






occur from the 


vomiting less 


more probable 






pain or asso- 


likely than with 


than in the 






ciated gastric 


biliary colic. 


other two. 






disturbance. 






Previous his- 


Of jaundice and 


Of gravel in urine, 


Of " bilious at- 




tory. 


similar attacks. 


or other patho- 
logical condi- 
tion of urine. 


tacks," if any- 
thing, or of 
dropped wrist. 


Age. 


Middle or later. 


Any age. 


Middle and 










young most 










likely. 



Chronic Obstruction of Bowels. — Previous history of notable 
irregularity of bowels ; rectal examination may give very 
important information ; possibly a tumour in known line of 
colon (malignant or intussusception). 

Typhlitis. — Pain usually correctly referred to right iliac fossa ; 
dulness on percussion and great tenderness, especially at 



SOME SYMPTOMS AND AFFECTIONS 



73 



M'Burney's point. If definite swelling and redness diagnosis 

nearly conclusive. 
Aneurysm. — Tumour has expansile pulsation ; pain more in 

back and worse at night ; bruit possibly heard over tumour. 

Vessels elsewhere degenerate : history of syphilis and hard 

work and alcohol probably. 
Caries. — Pain also referred to back, probably worse on jarring 

heels or tapping spine ; this or aneurysm may cause definite 

cord symptoms. 
Retroperitoneal Growth. — Only guessed at by excluding other 

causes for pain or cord symptoms. Possibly a tumour of 

irregular outline may be felt, lying deeply, and without 

expansile pulsation. 



DIARRHCEA AND CONSTIPATION 

The causes of these conditions or symptoms may thus be tabu- 
lated :— 



i. Contents of the gut. 
Too liquid. 



Too solid. 

Too irritating. 
Foreign bodies. 



2. Walls of the gut. 

(a) Ulcers : if not 
too deep to par- 
alyse. 

{b) Growths. 



(c) Inflammation. 



Clinical Illustrations. 

Doubtful if this condition per se ever causes 
diarrhoea, possibly excessive drinking 
might do it ; unduly active peristalsis may 
thus cause it by preventing absorption. 

Probably unusual sweating, habitual neglect 
of the bowels ; fever thus possibly causes 
constipation by too great absorption of 
water. 

Improper fermentation, unripe fruit or other 
indigestible material. 

Either by their presence cause irritation pos- 
sibly, or by their size cause obstruction, 
e.g. purgative drugs, or gall-stones, etc. 

Tubercular, typhoid, dysenteric, and simple. 



May cause irritation, and so diarrhoea, or 
paralysis, and so cause constipation ; 
sometimes by bulk or cicatrisation may 
also cause obstruction. 
.of peritonitis leads to paralysis, the most 



174 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



(d) Altered structure. 

(e) Altered circula- 

tion. 

(/) Blood conditions 
or toxaemias, 
which may either 
cause excessive 
peristalsis or ex- 
cretion into gut, 
or both, or, per 
contra, may act 
in the reverse 
manner. 

(g) Reflex nerve in- 
fluence, again 
acting either on 
peristalsis or 
secretion, or both. 

(h) Pressure from 
without acting 
mechanically or 
reflexly. 

(z) Some unexplained 



Clinical Illustrations. 

obstinate form of obstruction ; milder 
forms of this may by irritation cause 
diarrhoea, as in some cases of appendicular 
or cascal trouble. 

Lardaceous disease, leading to obstinate diar- 
rhoea. 

Heart disease, cirrhosis of liver, either con- 
stipation or diarrhoea. 

Bright's disease (uraemia) ; gouty habit ; 
probably some of the diarrhoeas of zymotic 
cases, critical or otherwise, are thus caused. 
Lead is the best known example of the 
opposite condition, viz. constipation. 



Cord diseases ; mental states, as fear, anxiety, 
insanity, etc., dentition in babies, com- 
monly causing diarrhoea, but not unfre- 
quently the reverse ; and here possibly 
may be placed the too solid motions of 
habitual neglect. 

If an abdominal tumour presses on the gut 
it is likely to cause constipation, but some- 
times it may cause diarrhoea reflexly, or 
by direct irritation. 

e.g. To what shall we attribute the almost 
universal constipation of the early days of 
sea-air, or other changes of climate and 
temperature ? 



The majority of the above cases offer no difficulty in diagnosis, 
for the constipation or diarrhoea is merely a concomitant symptom 
of some obvious disease or departure from the ordinary habits — 
dietetic, physical, or general — of the individual ; but a few guiding 
rules of procedure are required for the elucidation of those cases in 
which the diarrhoea or constipation is the only obvious symptom 
from which the patient is suffering, or, at least, of which he complains. 

In any such case the first and most important thing to ascertain 
is the precise meaning attached by the patient to the words he uses — 
ask how often the bowels act, whether much tenesmus or not, and 



v SOME SYMPTOMS AND AFFECTIONS 175 

the quantity and character of what passes, and inspect the motions 
for this purpose if necessary. A case recently has occurred to me 
in which the patient complained of an obstinate diarrhoea. Some- 
what puzzled by my ineffectual efforts at drug treatment, I was led 
to ask him to save everything passed for twenty-four hours ; I then 
found all the motions solid and natural, and further inquiry led to 
the conclusion that it was simply a case of a gross feeder whose 
bowels required naturally a more frequent relief. This inquiry and 
inspection will probably result in the discovery of any of the follow- 
ing conditions of the stools : — 

Natural in Consistency and Quantity. — As in the above case. 
If motions very narrow and ribbon-like, probably a stricture, 
organic or spasmodic (of sphincters), is present. 

Much Feculent Material, but too Watery, Light, or Dark. — If light 
or natural colour, suggestive of simple irritation of upper 
bowel by unsuitable food ; if dark and tarry, strongly sug- 
gestive of haemorrhage (q.v.), high up. 

Masses of Undigested Food or Curds (in Children), so-called Lien- 
tery. — Suggestive primarily of unsuitable or too free feeding, 
e.g. too much milk in typhoid ; and if this question is satis- 
factorily determined in the negative, then suggestive of 
undue nervous influences, perhaps best treated by bromides 
or nervine tonics. 

Pea-soupy Stools. — Might rouse a suspicion of insidious typhoid, 
and should lead to the use of the thermometer. 

Scybalous Knobs or very hard Fcsces ; probably with much Mucus. 
— Suggest a false diarrhoea, due to undue constipation ; 
hardening of the faeces ; a most important class of cases, 
because they are so common. 

Pus, or Pus and Blood; Mucus, or Blood and Mucus. — Rupture 
of an abscess into bowel. Much mucus is a pathognomonic 
sign of colonic trouble, and if present with hardened lumps 
almost certainly indicates constipation, either simple or due 
to organic obstruction, as the real trouble ; if with blood it 
is suggestive of dysentery, malignant or other stricture, piles, 
fistula in ano, etc. 

Membranous Masses floating in Water. — Membranous colitis ; in 
the absence of an acute illness rather suggestive of malignant 
disease, or occasionally chronic obstruction or simple con- 
stipation. 

The anus at least, and better also the rectum, should then be 



176 DIFFERENTIAL DIAGNOSIS chap. 

inspected and examined to see if any pathological condition is there 
present which can cause diarrhoea, or at least explain the patient's 
complaint, thus : — 

Piles or Simple Polypi. — May explain blood and mucus, excessive 
straining pain, etc. 

Fistula. — By its discharge may have given a false impression of 
diarrhoea, as well as altering the material of a stool. 

Ballooning. — If well marked is strongly suggestive of a stricture 
just out of reach, or that can with an effort be just touched. 

Stricture. — Malignant, syphilitic, etc., will explain either diarrhoea 
or constipation, or a marked alternation of the two con- 
ditions. 

Rectum full of Hardened Faces. — A very common thing to find 
in complaints of either diarrhoea or constipation. It must 
be emptied, and then a fresh examination made, as the 
condition may be a simple one, or it may be merely a symp- 
tom of some serious trouble to be discovered by the ex- 
amination of the empty viscus. 

Uterine and Ovarian Troubles. — In women a rectal examination 
is often required as well as vaginal ; it is possible for almost 
any organic disease or pathological position of the genitory 
organs to cause a disturbance of defaecation. 

A systematic examination of the abdomen, which may precede 
or follow the rectal one, may very likely reveal an efficient explana- 
tion of the trouble. Almost every pathological condition of the 
abdominal viscera may cause alteration in alvine evacuation, e.g. 
liver diseases (a.v.), splenic enlargements, any abdominal tumour, 
dilated stomach (q.v.), tubercular peritonitis, or any other form of 
peritonitis, or ascites, etc. ; as, however, most if not all of them 
will have given rise to complaints other than of diarrhoea or con- 
stipation, they will not here be further considered. 

Should the history and examination thus far have left matters 
still in doubt, the patient must next be thoroughly overhauled for 
evidence of some general disease, or a local one not situated within 
the abdominal region, which may be associated as cause with the 
symptoms under consideration. These are chiefly phthisis, lard- 
aceous disease, plumbism, Bright's disease, typhoid, leucocythaemia, 
and other blood dyscrasias or definite disease of the spinal cord or 
brain. 

These, like the troubles mentioned in the preceding paragraph, 
hardly require in this connection any further mention. The chronic 



v SOME SYMPTOMS AND AFFECTIONS 177 

cachexia, or suppuration, with the enlarged spleen and urinary con- 
dition of lardaceous disease ; the blue line, colic, and occupation 
of plumbism ; the temperature of typhoid ; the blood of leucocy- 
thaemia and anaemia; the low specific gravity and diminished 
urine of approaching uraemia (the diarrhoea is really a uraemic 
phenomenon) ; these are all sufficiently distinctive ; and so are the 
physical signs in the chest of a phthisical patient ; but it must not 
be forgotten that in consumption there are several possible sources 
for the diarrhoea which require a little consideration, owing to their 
importance ; thus : — 

Causes of Diarrhoea in Phthisis 

(a) Accidental, as it were, due to food, or change in climate, 

etc., from which phthisis confers no immunity. This 
may be sharp while it lasts, but is quite temporary, 
rapidly ceasing or yielding to treatment. Some change in 
residence or diet will probably give the clue to its origin. 

(b) In association with the dyspepsia, which is such a trouble- 

some accompaniment of phthisis, particularly in its earlier 
stages. In fact, when lung mischief is doubtful but sus- 
pected, this dyspepsia is a very suspicious piece of diag- 
nostic evidence. 
(<r) Due to tubercular ulceration of intestine. Usually occurs 
in later stages, when the lung trouble is very distinct. 
Associated with slight colicky pains, and very intractable 
to treatment, though often ceasing spontaneously. The 
presence of the ulceration cannot be diagnosed with 
certainty, but pain, and especially tenderness in the abdo- 
men, are suggestive when in combination with an obstinate 
diarrhoea. 

(d) Lardaceous changes supervening ; painless in itself, absolutely 

rebellious to treatment ; associated with distinctive signs of 
lardaceous trouble already mentioned in spleen and liver, 
and possibly kidney. 

(e) That of exhaustion in the very last stage of the disease ; the 

active cause, in fact, of the fatal ending in many cases not 
apparently due to either (c) or (d). 

Ascites 

The methods to be adopted to determine the presence of excess 
of fluid in the peritoneal cavity are so distinctly laid down in all the 

N 



178 DIFFERENTIAL DIAGNOSIS chap. 

text-books that I do not propose to discuss them except in tabular 
form, to separate ascites from cystic formations in the abdomen 
{vide p. 181). 

The causes of ascites recognised at the bedside belong to only 
two categories, or perhaps three, if we include chylous ascites. 

A. Irritation of the membrane itself — 

/Tubercle ~\ Either of the mem- 

-d J Carcinoma (secondary) ( braneor of an organ 

^ J Sarcoma (primary or second- C covered by it, e.g. 
v ary) / ovary, etc. 

Inflammatory affections of the peritoneum apart from 
growths rarely cause marked effusion, unless in conjunction 
with severe kidney mischief. 

B. Undue pressure of blood in the portal system, which may 

arise from — 

i. Local Causes in Abdomen, practically confined to the 
Liver and its Fissures, e.g. cirrhosis of liver, alco- 
holic or otherwise ; perihepatitis ; glands or 
growths (including a gall-stone very rarely) in the 
transverse fissure, whether primary or secondary. 
2. Produced by a Pathological Condition of other Organs — 
Either secondarily through the right 
heart, or by extension of growths and 
Heart inflammation from the pleura through 

Lungs -^ the diaphragm. When due to kidney 
Kidneys trouble, it arises probably from altera- 
tion in composition of blood, not from 
pressure. 

C. Undue pressure upon the receptaculum chyli or the thoracic 

duct, leading to transudation of a milky fluid into the peri- 
toneum-chyle. 

To determine to which of these primary groups a given case of 
ascites must be referred is usually a comparatively easy task ; to 
further differentiate the precise individual cause at work is more 
difficult, and often impossible, without exploration. 

In practice one usually first proceeds to exclude Group B 2. 
The history of the onset of the swelling of abdomen will here give 



SOME SYMPTOMS AND AFFECTIONS 



79 



us very important information — whether, that is, the ascites was 
the first complaint, or whether the patient had long suffered from 
other troubles, such as cough, or shortness of breath, puffiness of 
face or limbs, etc. A careful examination of the thorax and of 
the urine will then speedily give us either a negative or positive 
result. If the thoracic organs and the urine are found to present 
no morbid features, we may be at once sure that some local-abdo- 
minal cause is at work. Should any of them, on the other hand, be 
found in a markedly pathological condition, we know at once that a 
powerful accessory factor is present in the case, whether local causes 
are at work or not. The indications from the above examination of 
the thoracic organs will rarely if ever be of doubtful significance, for 
ascites does not arise from such causes alone until and unless they 
are of pronounced severity. 

To ascertain the exact local cause at work it is certainly 
advisable, and, if much fluid is present, often necessary, to empty 
the abdomen. 

In my opinion, this should always in the first instance be done by 
a small surgical incision, and not by a trocar, however small : (a) 
it is more scientific ; (b) safer for the patient ; (V) gives more informa- 
tion as to the exact condition of affairs ; (d) it has been known to 
cure cases otherwise deemed incurable ; (e) it allows at one operation 
removal of a removable cause should such be found. 

The character of the fluid (in whatever way it be obtained) will 
at once detect chylous ascites. A microscopic examination must 
be made for this purpose, not only to differentiate fat droplets from 
pus corpuscles, but also for the further intention of deciding the 
possible presence of cells of heterotopic character. (Physiological 
injections into animals will, if necessary, detect tubercle.) Should 
chyle be present, we know at once that we have to deal with a 
growth, either malignant or glandular, or possibly (very rarely indeed) 
with a blood parasite — Bilharzia or Filaria. 

Should the fluid prove to be clear or purulent, we have to deal 
with one of the causes in Group A or B (i). Purulent peritonitis is 
almost invariably associated with (a) severe kidney disease, which 
will have been already detected; (b) perforation of a viscus, the 
occurrence of which will have been only too obvious ; or, (c) in 
women, extension from vagina, uterus, or Fallopian tubes, a mode 
of production always to be suspected in the sex if no other cause is 
ascertainable. If the fluid has been obtained by incision, this will 
by itself have probably completed the diagnosis, but if circumstances 
should have prevented exploration, the following are the principal 



180 DIFFERENTIAL DIAGNOSIS chap. 

diagnostic factors, attention to which, in addition to what has been 
said already, will usually clear up the case : — 

Tubercular Peritonitis. — History of vague attacks of colic and 
irregularity of bowels. Abdominal walls probably feel thick 
to pleximeter finger or examining hand ; increased resistance. 
Irregular masses, with equally irregular dulness, may be 
appreciated. Patient usually young, though (even old) age 
does not exclude tubercle. 

Carcinoma. — Physical signs almost identical with tubercle in the 
small nodular form, and even on the post-mortem table the 
two may very closely resemble one another. More com- 
monly the primary growth is obvious as a tumour — ovarian, 
gastric, renal, etc. 

Sarcoma. — If secondary, indistinguishable from carcinoma for 
clinical purposes. If primary (of omentum) a tumour will 
be felt giving a sensation to examining hand identical with 
ballottement of pregnancy. Under thirty-five this cause 
may be almost at once excluded. 

Acute Inflammation. — Recognised by the great pain and tender- 
ness on palpation ; board-like muscles {vide purulent effusion 
above). 

Cirrhosis of Liver. — Admitted history of alcohol, or if not of 
alcohol then of morning vomiting ; possibly piles or haema- 
temesis. Liver usually enlarged, but surface regular, or at 
least without large bosses of carcinoma. 

N.B. — Youthful age does not exclude this cause, unfor- 
tunately. 

May be a history of syphilis, which points either to 
cirrhosis, gumma in portal fissure, enlarged glands, or peri- 
hepatitis. 

Perihepatitis. — To me, as an independent affection this is 
unknown, but I have seen it in connection with chronic 
peritonitis of tubercular or malignant origin, and also with 
syphilis and with heart disease. It is to be thought of when 
in a case of morbus cordis ascites is the prominent back pres- 
sure symptom, but I do not believe that it ever arises or 
causes trouble as a primary and separate disease. 

Glands and Growths in Portal Fissure. — If they cannot be felt, 
will only be diagnosed by a process of exclusion of other 
troubles ; but when the cause of ascites, can usually be felt after 
withdrawal of the fluid. 



SOME SYMPTOMS AND AFFECTIONS 



181 



Palpation. 



Percussion. 



Cystic Tumours, or Encysted 
Fluid of Ordinary Origin. 

Inspection of ab- Symmetry usually main- Usually some definite 

asymmetry to be per- 
ceived ; flanks do not 
bulge particularly. 
Tumour or tumours to be 
distinctly appreciated ; 
possible mobile, and 
feel cystic and fluctuat- 
ing. 
Dulness usually only 
appreciable over the 
tumour, not specially 
in flanks ; if it shifts 
with position of patient 
there is a perceptible 
movement of some- 
thing inside the ab- 
domen, detectable by 
palpation also. 

Thrill. Frequently to be de- Usually not obtainable at 

all ; if it is so, it will 
only be in a limited 
area through the body 
of the cyst, not through 
the whole abdomen. 

Other means. In females bimanual Bimanual in a female 

shows movements of 
uterus with ovarian 
cyst ; other cystic for- 
mations may be felt 
definitely as such, of 
limited extent or mobi- 
lity, or both. In ovar- 
ian cyst menstrual 
irregularities may also 
help us. 

The only case which is likely to cause much trouble is that of a 
large, thin-walled ovarian cyst, which has practically filled the whole 
abdomen. Here even a careful attention to the above points may 
still leave us in doubt. The history of menstrual irregularities, and 
of a previous asymmetry, together with an absence of all presumable 



Free Ascitic Fluid. t 

Symmetry usually main- 
tained ; flanks usually 
bulge markedly. 

No tumour to be felt, or 
if so it is a hard, solid 
mass. 



Dulness, particularly in 
the flanks with patient 
on back, possibly only 
here appreciable, and 
definitely shifts by 
imperceptible move- 
ment as the patient 
shifts his position. 



Frequently to be de- 
tected through the 
whole abdomen. 



In females bimanual 
examination gives no 
very distinctive infor- 
mation. 



1 82 DIFFERENTIAL DIAGNOSIS chap. 

causes of ascites, will probable put us right ; such cases are nowa- 
days very rare, and, of course, they can only occur in the female sex. 
Very great obesity of the abdominal wall is a great obstacle to phy- 
sical examination, and such a case demands extra care, with which 
difficulties may vanish, but frequently only an examination under a 
general anaesthetic will clear up a doubtful abdominal case. 

Simple Dyspepsia v. Gastric Ulcer 

Even in an elementary work dealing with diagnosis it seems 
impossible to omit all reference to this subject, for the cases are 
so common in which we desire to have guidance, and yet the 
definite separation of the two conditions — perhaps it would be 
more correct to say the exclusion of ulcer — is so extraordinarily 
difficult, that I feel it is much easier to criticise the criteria 
mentioned in text-books than to offer any distinction of my own. 

If we take a number of cases of gastric ulcer, either proved such 
by autopsy or diagnosed as such during life, we find the following 
points more or less marked : — 

i. The subjects will roughly divide themselves into two groups : 
(a) those whose ages range from seventeen to thirty ; (b) those from 
forty onwards. Group (a) will be almost entirely composed of the 
female sex, and the majority will have suffered from anaemia, and 
they will not have wasted. Group (fi) will be composed of either 
sex indifferently : anaemia — except for haematemesis — will not have 
been marked, but loss of flesh will commonly have appeared. 

2. Severe pain will have been a prominent feature in the history 
of the illness, and this pain will have frequently displayed the 
following peculiarities : — 

(a) Caused only by taking of food. 

{b) Appeared some little time after the ingestion of food, not 
at once. 

(c) Localised to a limited area, usually in the epigastric 

angle. 

(d) Increased by pressure on the spot, and often only then 

apparent. 

(e) Relieved almost immediately by vomiting when this has 

occurred. 

3. Vomiting is also likely to have been frequent, with chief 
characteristics : — 

(a) It occurred rather late after food. 



v SOME SYMPTOMS AND AFFECTIONS 183 

(b) It relieved the pain almost at once. 

(c) It has been actual blood or blood-tinged at least once. 
4. In the cases fatal from ulcer there will almost invariably have 

been, in addition to the above : — 

(a) Perforation with acute peritonitis ; or 

(b) Very severe hsematemesis ; or at least 

(c) Such constant severe pain and vomiting as to have led 

to death by exhaustion — this last mode of death is 
commoner in the group of older patients. 

Hence with regard to diagnosis it is very easy to say that an 
ulcer is present when the above symptoms occur in typical severity. 
It is the converse of this proposition, viz. to exclude an ulcer when 
gastric symptoms are slight, that offers such enormous difficulties ; 
in fact, there can be no hesitation in saying that it is impossible by 
clinical methods alone to prove this negative. Will the Rontgen rays 
here again help us ? 

It is being constantly proved in cases that are operated upon 
for perforation, less commonly in ulcers found on autopsy, that pain 
may be — 

{a) So slight as to be practically unnoticed. 

(b) Relieved by taking food. 

(c) Generally diffused and not localised. 

(d) Unrelieved, or only very gradually so by vomiting. 

That vomiting may be — « 

(a) Absent altogether. 

(b) Not bloody nor blood-stained. 

In fact, that in certain cases every one of the guiding indications 
may have been absent, or what is perhaps worse, may have been 
absolutely contra - indicative. These exceptional cases are far 
more common in the group of young subjects ; in the older group 
the features are more constant, though not even there entirely 
without exceptions. 

Dr. S. Fenwick has adopted, if not invented, a simple method 
of attempting to solve the diagnosis by getting the patient to 
swallow about a drachm of common salt in a tumbler of water when 
the stomach is empty ; should an ulcer be present, the salt coming 
in contact with a raw surface will excite a lively attack of pain ; if 
ulcer be not present, pain is not likely to be caused by the simple 
procedure. The same plan may be adopted to determine whether 
an ulcer, which has been diagnosed as present, has healed. 



1 84 DIFFERENTIAL DIAGNOSIS chap, v 

Apart from this clinical manoeuvre we can, I think, only lay 
down the following rules : — 

i. Never to think too lightly of an attack of dyspepsia in a 
young woman, especially if she be anaemic as well. 

2. Whenever it is possible, even at some inconvenience to the 
patient, to insist on a soft diet and a few days' rest in bed in all 
cases of dyspepsia which have not arisen from a fairly definite 
cause. 

3. A persistent-local (epigastric usually) pain in an older patient 
must similarly put us on our guard, to insist upon treatment appro- 
priate to ulceration. 

By attention to these rules we may cause some trouble to 
ourselves and our patients, but we shall at least have the satis- 
faction of having avoided anything likely to make matters worse. 



CHAPTER VI 

DISEASES OF THE URINARY ORGANS 

One of the most striking facts about kidney troubles is the fre- 
quency with which they occur without local symptoms. In acute 
nephritis it is true that aching pain in the loin is frequently present, 
and new growths of the kidney, including stone under that head, are 
usually associated at some period of their growth with more or less 
severe local pain : but chronic Bright's disease, lardaceous degenera- 
tion of the kidney, and, in fact, the majority of those cases in which 
the most serious degeneration and disintegration of the kidney 
structure are present, only betray themselves by general symptoms 
due to imperfect depuration of the blood, and by alterations in the 
urine of such a character, or so insidious in onset, that they may 
not have attracted the attention of the patient. 

For a discussion of the general symptoms refer to the heading 
Uraemia. The alterations in the urine are sometimes sufficiently 
obtrusive to be called symptoms, sometimes so insidious that they 
must be relegated to the class of physical signs, but in either 
instance they are so exceedingly important that they must be rather 
fully discussed for diagnostic purposes. 

Before we can appreciate or estimate pathological changes in the 
urine we ought to have a satisfactory general idea of the quantity 
and quality of the healthy excretion, and also of its physiological or 
healthy variations — a subject, which long experience of students has 
taught me, is dreadfully neglected, and forgotten as soon as the 
examination in physiology is passed. 

Normal Urine 

Should possess the following characteristics : — 

Quantity. From forty to fifty ounces in the adult. 

Appearance. Clear and bright. 



1 86 DIFFERENTIAL DIAGNOSIS chap. 

Colour. Amber to sherry, light or dark. 

Reaction. Acid. 

Sp. gravity. 1015 to 1025. 

It should, in an adult, be passed about four or five times in the twenty- 
four hours, and should on analysis show about 2 per cent of urea. 

The colour is due to various urinary pigments, ultimately, no 
doubt, derived from bile pigments and from haemoglobin. 

The reaction is due to the presence in fairly large quantities of the 
acid phosphate of sodium NaH 9 P0 4 {and probably of the analogous 
potassium salt also in smaller quantities}. It is truly wonderful how 
this simple, well-established fact is forgotten by students, who will 
persist in ascribing the acidity to uric and hippuric acids, regardless 
of the feeble acidity of these bodies, and their insignificance in 
quantity. 

Variations in Health 

In health the following are the chief factors influencing the 
urine, and a brief epitome of how and why. 

1. Exercise. — Physical work must undoubtedly — by mere wear 
and tear of fixed tissues as well as by quickening circulation, and 
therefore oxidation of more floating capital — have a tendency to 
throw more waste products into the blood. These waste materials 
are the ultimate oxidation products of organic food stuffs, H 2 0, 
C0. 2 , and urea or uric acid (as urates) ; the H 2 and C0 2 pass off 
in large measure through the lungs by increased respiratory move- 
ment, and through the skin with the sweat, which is also markedly 
increased by exercise ; hence there follows as a natural deduction, 
just what is seen in actual practice, viz. that with exercise the urine 
shall as a rule be lessened in quantity, but increased in specific 
gravity, by a higher proportion of nitrogenous waste material and 
inorganic salts. 

At first this nitrogenous waste takes the form of uric acid, so 
that a copious deposit of urates and biurates is the familiar result 
of a hard day's work in one who is unaccustomed to physical 
labour. As uric acid is a less oxidised product than urea, i.e. 
contains a smaller proportion of oxygen, it is probable that this 
deposit is due in some way to an inefficient supply of oxygen to 
burn up the increased waste suddenly produced. When the body 
has had time to accommodate itself to the circumstances, the more 
usual metabolism of nitrogenous waste into urea again comes to the 
fore. 



vi DISEASES OF THE URINARY ORGANS 187 

2. Food. — The ingestion of food influences the urine in two 
ways : — 

A. Directly : by the simple excretion of excess of water taken 
in — the student is apt to forget that the so-called solids of the food 
(a) contain a large proportion of free water, (b) produce much water 
by their oxidation, so that it is not only the drink alone of the food, 
but the solids also that produce this excess. 

B. Indirectly : during gastric digestion a quantity of HC1 is 
required, the manufacture of which sets free a corresponding 
quantity of sodium in the blood, with the result that the phosphate 
of sodium in the urine is more likely to become Na 2 HP0 4 , or even 
NagPO^, rather than NaH 2 P0 4 . 

By both these processes, then, the quantity, the specific gravity, 
and the acidity of the urine are likely to be influenced — the first in- 
creased, and the last two diminished ; the acidity to such a degree 
that it is quite within physiological limits to find the urine neutral 
or even alkaline after a full meal. 

3. Weather. — This simply has reference to the temperature 
to which the skin is exposed when no compensating influences 
— such as exercise — are at work on the circulation through it. 
Cold causes the skin to contract, and diminishes consequently 
its circulation and excretion of sweat, with the result that the 
amount of urine passed is increased ; external heat will have the 
contrary effect. 

4. Mental Conditions, such as fear, certain hysterical states on 
the borderland of health, and especially doubt as to opportunities 
for voluntary micturition, undoubtedly have an influence on the 
secretion of urine ; but their exact mechanism is obscure, and we 
can only record the fact. 

Thus we see that — 

^ U y ' J May all be profoundly altered by exercise, food, 

•d J' I weather, and mental conditions. 
Reaction, y ' 

We will now proceed to discuss from a diagnostic point of view 
the variations in urine due to disease. 



ss 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



Variations in Disease 
Increased Frequency of Micturition 



May to due to — 
. Acute inflamma- 
tion or irritation 
of kidney. 
, Stone, or other 
growths of kid- 
ney, with colic. 
Cystitis and 
bladder calculus. 



Prostatic troubles. 



5. Polyuria. 



Chief diagnostic points. 

Very small quantities at a time, total quantity 
much diminished, probably blood in it ; stran- 
gury not infrequent. 

Also like acute inflammation, but with severe pain 
(renal colic, q.v.) probably running down into 
groin. 

Total quantity probably about normal, possibly 
alkaline and ammoniacal, certainly much mucus 
deposit ; probably pain in bladder or perineum, 
which may only be at end of act, and often 
referred to the glans penis. 

If acute the act is itself very painful ; if chronic 
the increased frequency of micturition is chiefly 
at night, with possibly some difficulty in starting 
the act during the day, and the catheter 
(possibly passed with difficulty) shows residual 
urine ; total quantity normal or greater than 
usual. 

Vide next section ; total quantity much in- 
creased. 



1. Acute congestion 

or inflammation, 
if primary. 

If on the top of 
old mischief. 

2. Large white kid- 
ney. 

3. Blocking 
ter. 



of ure- 



4. Retention, heart 
disease, and gen- 
eral circulatory 
disturbances. 



Total Quantity 
Is Diminis/ied in 

Frequent micturition ; strangury • smoky or 

definitely bloody urine ; albumen and casts ; 

possible history of turpentine or copaiba, etc., 

administration. 
The same features, but with history of previous 

increased quantity. 
Vide section on L.W.K. Urine nearly solid with 

albumen ; patient very anaemic. 
If of both, total suppression {q.v.) ; if one only, 

such urine as escapes possibly normal; probably 

severe pain in groin and loin. 
Vide Suppression v. Retention, p. 216. Moderate 

quantity of albumen ; history of gradual 

diminution in quantity of urine, and presence 

of other signs of heart disease or circulatory 

disturbances. 



DISEASES OF THE URINARY ORGANS 



Is Increased in 



Cirrhotic kidney. 



Consecutive neph- 
ritis. 

Lardaceous kidney. 



Hydronephrosis. 



Diabetes insipidus. 



Diabetes mellitus. 



Hysteria, after rigors 
of malaria, occa- 
sionally after 
crisis of acute 
\ disease. 



Low specific gravity, little albumen, patient 
probably over forty-five years of age ; few 
if any casts. 

Probably considerable number of casts ; 
fair quantity (up to one quarter) albumen, 
and history of acute kidney trouble. 

Probably also enlarged spleen and liver, 
and known cause of lardaceous degenera- 
tion present ; albumen considerable, casts 
may or may not be numerous, and 
possibly show lardaceous microscopic re- 
action. 

Increased quantity only at irregular intervals, 
and urine quite likely without much change 
from normal ; abdominal tumour in renal 
region often detectable. 

Quantity enormous, up to 300 or 400 ozs. ; 
specific gravity very low ; absence of albu- 
men or other pathological constituent. 

Specific gravity usually above 1025, but, N.B. 
— sugar may be present in urine of specific 
gravity below 1020; presence of sugar; 
urine of peculiar appearance and general 
symptoms of diabetes. 

Urine offers no special peculiarities ; the 
polyuria is quite temporary, and the 
attendant circumstances are quite sufficient 
for diagnosis. 



Colour 



Of pathological variations in colour due to changes in the 
urinary pigments very little is known, and still less use can be 
made for clinical purposes of the knowledge we do possess (perhaps 
with the exceptions of melanin and indican); but the follow- 
ing substances when present will produce evident colour variations 
from the ordinary, and these variations form the first preliminary or 
simple test for the respective substances, and should therefore be 
remembered : — 



190 



DIFFERENTIAL DIAGNOSIS 



Bile pigments. Urine a yellowish green tinge in thin layers, 

almost black in thicker ones ; if shaken the 
froth possesses a beautiful yellow colour. This 
yellowness of the froth is pathognomonic of bile 
in urine (? rhubarb or santonin). 

Blood. Urine either of a smoky tinge and not clear, or 

possesses the red colour of blood more or less 
marked. 

Chyle. Urine distinctly milky throughout, and often co- 

agulates into a soft jelly. 

Carbolic acid. Urine of a green colour, looking almost black in 

thick layers. 

Rhubarb. Brownish yellow colour, becoming red on adding 

alkali, disappearing with an acid. 

Santonin. Bright yellow ; disappears with free acid. 

Hcematoxylin. Reddish, also disappears with free acid, thus 

differing from red colour due to blood ; vide 
Hematuria. 

Iodides and bromides. Dark colour appears on adding nitric acid, due 
to setting free of iodine or bromine. 

Methylene blue (occa- Urine of a bright blue colour. I have recently seen 
sionally given for a case of eosin in the urine mistaken for blood 
rheumatoid - arth- — it arose from eating sweets coloured with 

ritis). eosin. 

Specific Gravity 

Apart from the knowledge of the total quantity passed in twenty- 
four hours, variations in specific gravity have very little positive patho- 
logical significance. A high specific gravity (over 1027) should, 
however, at once rouse a suspicion of glycosuria {q.v.), while a low 
one (under 101 5) should immediately start inquiry into the total 
quantity passed, etc., leading in the direction of suspected cirrhotic 
kidney, unless other obvious explanation be at hand. 



Constituents of Urine not usually found in Health, 
and essentially pathological 



By their presence. 

Or by excess. 
Or by altered condi- 
tions of urine. 



Blood, pus, casts, sugar, albumen, chyle, phos- 
phate of lime if in quantity, bile. 
Urates, mucus. 
Triple phosphates, ammonia. 



For convenience of discussion, and because of its practical 
utility in urine analysis, we may divide these constituents into those 



vi DISEASES OF THE URINARY ORGANS 191 

which form, or are chiefly found in association with, a deposit of 
some sort, and those which still leave the urine quite clear notwith- 
standing their presence, thus : — 

Forming, or chiefly found in, a Deposit. Leaving the Urine clear. 

Phosphates of lime. Sugar. 

,, triple. Albumen. 

Urates and uric acid. Blood. [If in quantity 

Oxalates. Chyle, -j usually makes 

Mucus. Bile. urine opaque. 

Pus. 
Casts. 
Blood staining a precipitate. 

It is obvious that there are two questions requiring answers in 
connection with these abnormal constituents — 

( 1 ) By what tests shall we recognise them ? 

(2) What clinical diagnostic use can we make of the information 

thus acquired ? 

To the first of these questions I propose to give merely an 
outline of a reply; for details of manipulation special manuals 
must be consulted, as I am chiefly concerned with clinical and not 
scientific questions. 



Tests for the Nature of an Abnormal Constituent 
of the Urine 

There are three methods to be adopted in testing urine, all 
of which should be employed in turn as corroborating one another : 
(1) ordinary physical examination by the eye and nose; (2) chemi- 
cal experiments ; (3) microscopical investigation ; if very great 
accuracy is demanded, the spectroscope may be used to detect 
blood and bile. 

Smell 

Of ammonia. Indicates decomposition, and so far gives a clue 

to the improbability of a deposit being urates, 
but suggests pus or triple phosphates. 

Of violets. That the patient has been taking turpentine. 

These are the only two indications that smell is likely to give 
one, but asparagus and possibly other articles of diet do alter the 



192 



DIFFERENTIAL DIAGNOSIS 



natural smell of healthy urine, though the fact is not of much 
clinical value. 

Appearance to Naked Eye of Urinary Deposit or Urine 

Phosphate of lime , . 1 White, more or less granular deposit; some- 
times in large amount ( = phosphatic diabetes), 
and may be hummocky from intermixture of 
mucus. 

Triple phosphates." 1 Only recognised accurately by microscope in a 
deposit ; urine ammoniacal. 

Urates. Usually coloured pink or red ; if white they may 

be distinguished from phosphates by the fact 
that they usually adhere to the side of the 
vessel at the top of the urine. 

Uric acid. Only seen as isolated little cayenne-pepper grains 

at the bottom of the glass, or entangled in 
mucus. 

Oxalates. Usually seen (if at all by naked eye) as small 

shining crystals entangled in the mucus. 

Mucus. Practically a constant feature even in health ; it 

forms a translucent, semi-transparent, floccu- 
lent cloud towards the lower part of the 
glass, and often floating free in the middle of 
the urine. 

Pus. White or greenish white, often hummocky deposit 

at the bottom of the glass, not granular, but 
easily mistaken for phosphates or white urates ; 
mucus cloud usually excessive above it ; urine 
commonly, though by no means invariably, 
ammoniacal. 

Blood. Smoky or definite red colour of blood, light or 

dark. 

Sugar. Peculiar greenish yellow tinge in typical diabetic 

urine, but perhaps more often nothing very 
distinctive. 

Casts and Albumen. Only observable under the microscope ; not any 
characteristic appearance. 

Bile. Vide colour and chemical changes, p. 190 



1 Students are very apt to forget that phosphates of sodium and potassium are 
soluble in water, and therefore do not occur in precipitates. 

2 These crystals are called triple phosphates, because all three atoms of hydrogen 
are replaced by metals (2 by Mg, 1 by Am) ; they can only occur when decomposi- 
tion has taken place in the urine, either within or without the body ; for without 
decomposition ammonia does not appear in the urine. 



DISEASES OF THE URINARY ORGANS 193 



Heat and Chemical Tests 

First ascertain by litmus paper the reaction of the urine. Inas- 
much as all the deposits may occur in acid or alkaline urine, with 
the exception of triple phosphates {vide footnote, pp. 192 and 209) 
and excessive urates, an alkaline reaction gives no very definite 
information beyond a strong probability that a deposit is not urates, 
but it is important in the heat test for albumen. 1 

Then take a little of the urine in a clean 2 test-tube (if there be 
a deposit to be tested take care to get plenty of it in the test-tube), 
and apply heat very cautiously and gradually, watching the urine 
carefully all the time. Bring it to active ebullition, and finally add 
a drop of nitric or, better still, acetic acid. 

The meaning of this is as follows : — 

1. From cold up to, say, a little below blood heat urates will 
gradually dissolve : 

.-. Watch the deposit to see if it gets lighter — the diminution 
represents urates ; if no diminution up to this point, no 
urates ; and, N.B. — all urates are now dissolved, and so 
cannot be mistaken for albumen. 

2. From about blood heat up to boiling albumen will, if present, 
be coagulated and appear as a precipitate ; the more albuminous a 
liquid the lower the temperature at which the albumen will begin to 
coagulate : 

. •. Watch the deposit (or clear urine) to see if it gets thicker (or 
clouds). 

Any precipitate now appearing is either albumen or phos- 
phates, 3 and neither will disappear on boiling, so we add one drop 
of acid (acetic is best, as it is weaker and so avoids fallacies of 
nitric dissolving traces of albumen), which — 

3. Dissolves any phosphates, but (if not too much be added) 
leaves the coagulated albumen untouched : 

1 This is owing to the fact that when decomposition takes place any albumen 
present is converted by the ammonia into alkali-albumen, which is not coagulated by 
heat alone. 

2 Dirty test-tubes, especially with acid, will often prevent precipitation of 
albumen. 

3 It is doubtful to what cause this deposition of phosphates is due ; possibly escape 
of C0 2 which held them in solution, or possibly some subtler chemical change in them 
produced by boiling (Ralfe). 

O 



i94 DIFFERENTIAL DIAGNOSIS chap. 

.'. The part of final precipitate clearing up with acid = phos- 
phates ; remainder = albumen or other proteid body ; if 
brownish red, probably due to blood or stained by blood. 

4. If the deposit is unaltered or only slightly thickened by boiling, 
it is either phosphates or pus. 

Now take a fresh specimen in a clean test-tube, and add a drop 
or two of acetic acid or weak nitric acid, this — 

Makes mucin stringy ; 
Dissolves phosphates ; 
Does not affect urates ; 
Does not materially affect pus. 

To a similar specimen add a few drops of caustic potash ; this — 

Causes pus to become jellified or ropy ; 

Dissolves urates ; 

Does not affect urates markedly. 

To test for sugar, boil some Fehling's solution, and while 
boiling hot add a few drops of urine ; if sugar be present, red or 
yellow oxide of copper is rapidly precipitated. There are many 
other tests for sugar, and great controversy still exists as to which 
is the best ; but the above, known as Fehling's test, is sufficient 
and accurate enough for ordinary clinical purposes. 

If bile be suspected by the colour, Pettenkofer's test with fuming 
nitric acid, giving a play of colours if bile pigments be present, may 
be applied as confirmatory evidence. But the simplest of all tests 
for bile is the yellow colour imparted to the froth that appears 
when urine is shaken. 



Microscopical appearances of Urinary Deposits and Elements 

Oxalates. 

Phosphates — Amorphous or crystalline. 

Triple phosphates. 

Pus. 

Blood cells. 

Urates. 

Uric acid. 

Casts. 



DISEASES OF THE URINARY ORGANS 195 



CLINICAL SIGNIFICATION OF ABOVE 

We may now proceed to discuss more fully the second question 
mentioned above, viz. What is the clinical significance of the various 
morbid constituents, and how far are they of diagnostic value ? 



Albuminuria 

The causes that may produce albumen in the urine are many, 
but we can distinguish in clinical work three groups of albuminuria : — 

Group I. — In which the albumen is only a sub- Blood {vide Hasma- 
sidiary factor, and its presence completely turia). 

accounted for by the other constituent, viz. — Pus {vide Pyuria). 

Spermatorrhoea (?). 
Group II. — Present With abundant casts, indicating acute kidney 
with other factors disease, or consecutive nephritis in earlier 
explaining its an- stages, 

atomical source, 
viz. — 
Group III. — In Cirrhotic kidney. 

which it is often Consecutive nephritis in later stages, 
the only obvious Lardaceous kidney, 
morbid constitu- Surgical kidney (hydro-nephrosis). 
ent, though a few Stone in pelvis, probably with pus or crystals, 
casts or crystal- Cardiac disease or general back pressure, 
line substances Abdominal disease or pregnancy, with local back 
may be present in pressure. 

some cases. With or after some specific fevers — diphtheria, 

scarlet fever, etc. 
So-called cyclical or functional albuminuria. 
Leucorrhea in women. 
Anaemia (occasionally). 
Debility in or after many general diseases. 

To determine to which of these groups a given case belongs it 
is obvious, then, that we must examine the urine carefully (and 
repeatedly in some cases) by chemical and microscopical 1 tests. 

1 If no obvious deposit is present let the urine stand for twelve hours in a conical 
vessel covered from dust. The late Dr. Ralfe used also to dust a little powdered 
starch on its surface, to carry down mechanically any floating casts. If a centrifugal- 
ising machine is available this is the best method of obtaining a deposit. 



196 DIFFERENTIAL DIAGNOSIS chap. 

These will be practically certain to differentiate Groups I. and II., 
and by exclusion lead us to believe that some member of Group III. 
is causing the mischief. 

Then note the quantity of albumen present ; if only a trace, it 
is most likely due to — 

Cirrhotic kidney. 

Back venous pressure (local or general). 

Surgical kidney (first or second stage, q.v.\ 

Specific fevers (not reaching stage of actual nephritis). 

Leucorrhea. 

Anaemia. 

Cyclical or functional (q.v.). 

If more than a trace, probably — 

Lardaceous kidney, or 

Consecutive nephritis without many casts, or 

Chyluria. 

Most of these conditions will become tolerably obvious when 
the patient as well as his urine is carefully overhauled, but one or 
two of them require a little further consideration. 

Cyclical or Functional Albuminuria 

These are terms invented to describe cases which were, I 
believe, first noticed by examiners for life assurance (but the con- 
dition has subsequently been investigated by many observers), who 
found albumen in the urine without obvious cause, and with an 
entire absence of other guiding pathological constituent or even 
symptom. Its exact pathology, and above all its precise clinical 
significance from a prognostic point of view, are still but imperfectly 
understood, but before we can allow ourselves to rest content with 
such a diagnosis, the following propositions and conditions must 
have been rigorously investigated : — 

i. That the patient must have been most carefully examined in 
every system, without finding evidence of disease (more especially, 
perhaps, the condition of the vascular system). 

2. That the urine and the urinary system must have been also 
repeatedly and carefully examined without the discovery of any 
morbid constituent or local condition, especially casts, blood, pus, 
stricture, stone, phimosis, leucorrhea, fever, phthisis, leucocythsemia, 
etc. 



vi DISEASES OF THE URINARY ORGANS 197 

3. That the albumen shall never have been more than a trace. 

4. It is a condition hitherto found almost exclusively in 
adolescents (boys or girls), or youngish adults, though it is uncertain 
how far it may persist into later life. 

5. The circumstances found to influence the presence and 
quantity of the albumen have usually been position of body, exer- 
cise, exposure, and certain articles of diet, e.g. eggs ; and hence the 
urine must be examined on several occasions — 

Before and after rising in the morning ; 
„ „ cold bathing; 

„ „ food of suspected kinds ; 

„ ,, exertion (slight and severe). 

If these various testings give various results while other condi- 
tions remain the same, a preliminary diagnosis of functional may 
be given, but one to be willingly abandoned on the discovery of 
some indisputably organic change. 

Surgical Kidney as Cause of Albuminuria 

Surgical kidney is a convenient, but somewhat invidious, expres- 
sion used to denote a kidney which has been damaged by obstruction 
to the free outflow of urine from its pelvis. It would appear that 
an intermittent obstruction is equally, if not more, efficacious than a 
permanent one in producing the condition. 

In its typical form it is essentially a surgical trouble with surgi- 
cal treatment, and its description and discussion must be looked for 
in surgical manuals ; but as its earlier manifestations and irregular 
forms may easily come before a physician, its main features are here 
glanced at. 

There are three forms or stages of it readily distinguishable 
when met with alone, but they are far more usually — on the post- 
mortem table at any rate — mixed with one another : — 

1. Simple atrophy of pyramids from pressure. 

2. No. 1, plus chronic inflammation of kidney from irritation. 

3. No. 1 and No. 2, plus septic infection of the urinary tract. 

As regards the causation, there are three well-known causes, viz. 
stricture of urethra, stone in the bladder, and enlarged prostate, 
and when either of these is in operation it is probable that both 
kidneys will suffer. The disease is here mentioned in a medical 
work chiefly on account of a group of cases which arise from very 



198 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



ill-understood causes that are supposed to give rise to intermittent 
kinking of the ureter, with a consequent intermittent increase of 
pressure in the pelvis. 

Definite diagnosis of such cases is in all probability impossible 
in their earlier stages, but the following symptoms would render the 
condition highly probable : — 

1. Albuminuria probably not more than a trace, and very pos- 

sibly intermittent. 

2. Marked irregularity in the quantity of urine passed in succes- 

sive days. 

3. The presence in the abdomen of a tumour, possibly ill-defined, 

diminishing and increasing according as the amount of 
urine passed is large or small. 
The remaining conditions of albuminuria in Group III. may be 
more briefly dismissed in tabular form : — 



Condition. 

Cirrhotic kidney, 
or consecutive 
nephritis in the 
later stages. 

Lardaceous kid- 
ney. 



3. Heart disease. 



Abdominal dis- 
ease. 

Neph rolithiasis. 

Diphtheria, scar- 
let fever, or 
other zymotic; 
ancemia, leucor- 
rhea, convales- 
cence from even 
acute nephritis. 



Guiding Indications. 

Specific gravity low ; quantity increased ; heart 
hypertrophied ; vessels probably degenerate ; 
distinct history of nephritis in consecutive 
cases. 

Albumen considerable ; quantity of urine greater 
than usual ; some obvious cause for lardaceous 
change, not forgetting syphilis and phthisis ; 
liver or spleen, or both, almost sure to be 
enlarged ; painless diarrhoea may (rarely) be 
present. 

Bruits probably present, or at least alterations 
from health in the cardiac sounds ; nearly sure 
to be oedema of legs ; quantity of urine dimin- 
ishing lately, pari passu with the onset of other 
back pressure symptoms. 

Ascites or tumour or pregnant uterus ; swelling 
of abdomen probably obvious. 

Vide Stone in Kidney. 

The history of such disease is usually obvious 
enough ; albumen likely to diminish as convale- 
scence proceeds, but casts must be anxiously 
looked for. 



In connection with all the groups, but especially perhaps with 



vi DISEASES OF THE URINARY ORGANS 199 

this last group, of causes of albuminuria, a very anxious question will 
often arise — Is this patient weak and anaemic because he is albu- 
minuric, or is he albuminuric because he is weak ? The question 
is important because of treatment. If we feed him up to cure 
anaemia we may further damage his kidneys : if we starve him to 
relieve the kidneys we may perpetuate the anaemia, and also the 
debility of renal tissue. To answer this question fully would require 
an essay, but the following points are worthy of attention : — 

It is obvious at once that all albuminuria depends upon and is 
caused by — 

(1) Acute or gross disease in or near 

(2) Simple nutritive (or original) debility of 

some part of the kidney structures, which, when healthy, prevents 
or does not cause a transudation of albumen into the excretion. 
Acute or gross disease includes — 

(a) All those cases (stone, tubercle, carcinoma, perirenal abscess, 
etc.), the treatment of which is or should be almost entirely surgical, 
and of which a brief note will be found under the appropriate 
heading. 

(b) Inflammation of the kidneys or bladder, of which, when 
acute, the treatment and management are obvious enough. 

Difficulties and doubts arise when the acute trouble has subsided 
and the case become one in which the albumen remains (with the 
anaemia in the secondary cases, possibly without it in the primary 
ones) as practically the only sign of disease. These must be placed 
for our present object along with the group in which no such acute 
local trouble has been present. The following important proposi- 
tions may then be made on them, each proposition having weighty 
therapeutical deductions : — 

1. Albuminuria of so-called functional or cyclical origin may 
exist for years without the subject of it showing any marked deterio- 
ration of health, and the same is true of many albuminurias which 
are the sequel of known acute Bright's or other gross renal 
mischief. 

2. If the urine on boiling becomes practically solid, this only 
means about 2 per cent of albumen — say the equivalent of an egg 
or a couple of ounces of beefsteak in twenty-four hours ; while what 
is ordinarily spoken of as a trace of albumen means from J to 
T \j- per cent or less — the equivalent of about one ordinary mouth- 



2oo DIFFERENTIAL DIAGNOSIS chap. 

ful of food — so that as a mere drain of nutrient material from the 
body albuminuria may be certainly neglected. 

3. Experience has shown, after many trials, that no drug and no 
plan of low diet expressly used, ad hoc, has hitherto been found 
capable of preventing or eliminating the last traces of albumen from 
the urine. 

4. It is the life-work of the kidneys to excrete some of the 
waste products from the body, and these oxidation products come 
from two sources : — 

(a) The result of the ordinary never-ceasing activity (life, growth, 
and decay) of all the body tissues and cells. 

(b) A possible, or even probable, luxus consumption of materials 
taken in by the mouth as food, but never really assimilated into the 
structures of the body. 

Now, any rational system of management of albuminuria must 
take all these facts into account. Wear and tear of tissues cannot 
be checked entirely, but it may be kept within moderate limits by 
avoiding excessive physical exertion. Luxus consumption can also 
probably not be entirely avoided, but may be reduced considerably 
by avoiding excess of nitrogenous food. Beyond these extremes I do 
not think we should be too strict either in diet or exercise with 
albuminurias, for constant worry of obeying rules is worse than 
occasional lapses from them. 

Pyuria or Pus in the Urine 

The sources of pus found in the urine may thus be tabulated, 
with their most prominent guiding features : — 

Source. Chief Points. 

Urethra, in either Quantity small ; escapes at any time, indepen- 
sex. dently of micturition, and stains and stiffens the 

linen ; micturition probably painful ; squeezing 
urethra towards meatus shows a bead of pus. 

Vagina infe?nale. Similar indications, and speculum clinches the 

diagnosis ; also vaginal epithelium revealed by 
microscope. 

Bladder. Most probably associated with frequent distress- 

ing micturition and other symptoms of cystitis ; 
urine possibly ammoniacal on voidance ; much 
bladder epithelium under microscope ; if no 
symptoms (or very slight) of cystitis, pus prob- 



DISEASES OF THE URINARY ORGANS 



Source. 



Ureter. 

Kidney and pelvis 
thereof. 



Chief Points. 

ably in small quantity, but the cystoscope must 
be appealed to as final arbitrator. 

Practically indistinguishable from kidney. 

Quantity usually considerable ; stone and tubercle 
most common causes ; urine most commonly 
acid, and but little disturbance in frequency of 
micturition, except in stone • pain of a colicky 
nature not unfrequent ; renal epithelium 
frequently found under the microscope. 



If we have ascertained the place of origin of the pus, the next 
point is the cause of the suppuration itself: — 



i. In urethra. Hunterian chancres have been known to occur in 

the urethra ; the finger would readily detect 
them ; instrumental irritation. 

Strain has lately been asserted on good 
authority to cause a urethritis independently of 
sexual connection. 

Gonorrhoea, recent or old (with stricture), is, 
after all, far and away the commonest cause. 
If the matter is legally disputed the gonococcus 
would be the only possible distinctive feature, 
though this is more likely to lead to hard 
swearing than to scientific conviction. 

2. In vulva and Such causes as foreign bodies (pessaries, etc.) are 

vagina. obvious on inspection with a speculum, as are 

also chancres, epithelioma, etc. 

It is indisputably proved that in young sub- 
jects dirt, masturbation, etc., may start a sup- 
purative inflammation without a suspicion of 
criminal violence. A diagnosis without a his- 
tory is impossible, but the fact of such vulvitis 
occurring must be remembered by a medical 
jurist. 

3. In Bladder. That suppuration may occur in the bladder, or at 

least that pus may enter the urinary tract at 
the bladder without general cystitis, is true ; 
but its occurrence is so rare that practically 
the causes of cystitis and of suppuration 
through or from the bladder are the same. 
They are : — 



DIFFERENTIAL DIAGNOSIS 



(a) Foreign 
bodies. 



(b) Distension 
from 



(c) Extension of 

inflamma - 
tion. 

(d) Debility. 



(e) Ulcers — 
Simple, tu- 
bercula r, 
malignant, 
primary, or 
extending to 
bladder from 
other organs, 
especially 
uterus. 
4. From kidneys 
and ureters. 



Stone.— Proved by the sound. 

Faeces or septic pus. — History of illness, such as 

typhoid, parametritis, pyosalpinx, which could 

give rise to entero-cystic fistula or abscess 

bursting into the bladder. 
Bits of catheter, etc. — History generally admitted, 

but may be only recognised by the sound. 
Stricture of urethra. — Proved by the catheter 

and history of difficult micturition. 
Enlarged prostate. — Found by catheter or finger 

in rectum. 
Simple atony. — Residual urine drawn off by 

catheter. 
Uterine enlargement or puerperium ; obvious. 
History of acute urethritis or vaginitis, possibly 

diphtheritic. 

Cystitis arises in the very old or very young, or in 
patients debilitated by any illness, from very 
trivial causes, entirely overlooked perhaps, and 
not operative in health, e.g. clean coitus, clean 
catheter. 

The tubercle bacillus or fragments of a neoplasm 
if present will, of course, settle the matter for 
two of these, but otherwise to be certain of 
them is impossible without the aid of the 
cystoscope. 



The causes of suppuration from kidneys and 
ureters are not very numerous. 



Tubercle. 



Stone. 



Principal Points 

Pus abundant (may be none, vide Tubercle of 
Kidney), and haemorrhage, too, not unfre- 
quent ; tubercle bacilli in pus ; renal colic not 
unfrequent ; possibly tubercle elsewhere. Age : 
middle life usually. 

Pus as a rule not very abundant ; colic common 
{vide Nephrolithiasis). Age : children and old 
people very prone to it, but no age exempt. 



DISEASES OF THE URINARY ORGANS 



!o 3 



Malignant dis- 
ease. 



Pyaemia. 



Perinephritic ab- 
scess. 



Pus not much ; haemorrhage more likely {vide 
Kidney Cancer). Age : late adult life, except 
rapidly growing sarcomata, which are almost 
confined to children. 

Either extension from the bladder, when the 
cystitis will mask the kidney symptoms, or a 
cause of general pyaemia present ; in either 
case renal features quite subordinate. 

History of increasing pain and swelling in the 
loin ; pus in urine increasing or diminishing 
with diminution or increase in tumour, and 
often quite intermittent. 



In all the above renal troubles if pain or tenderness be marked 
on one side, and not on the other, or if a very distinct tumour be 
felt by abdominal examination, the kidney at fault will easily be 
known ; but it is a very common thing for the diagnosis to remain 
in doubt until the cystoscope has been used, showing something 
abnormal in or of the ureteral orifice of the affected kidney. 

HEMATURIA 

Blood like pus may come from any part of the urinary tract, and 
in the main the indications of its source are similar. 



Urethra. 
Prostate. 



Chief Indications 

Is pure, and escapes at any time, thus staining 
the clothes ; probable history of traumatism or 
instrumentation. 

Blood from prostate either gets into the bladder, 
or trickles down the urethra ; in either case 
the prostate would only be suspected if other 
symptoms of enlarged prostate had occurred, 
or if digital or instrumental examination had 
revealed prostatic abnormalities. 



Table of Differences of Hematuria from 



Bladder. 
Usually very obvious blood ; often 



irregular clots in it 
quently by itself. 



blood fre- 



Kidneys. 
More commonly a smokiness, not 
obviously blood, more intimately 
mixed with urine ; if clots, they 
will have shape of ureter. 



204 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



Bladder. 
No renal casts ; possibly bladder 
epithelium. 

Strangury l a less common associa- 
tion. 

If any local pain it is in bladder 

region, or at end of penis. 
Never hemoglobinuria only. 



Kidneys. 

If from renal substance, almost in- 
variably blood casts of renal 
tubules. 

Strangury a common association, 
e.g. after taking turpentine or 
application of cantharides. 

If any local pain it is in renal region, 
or in groin and testes. 

May be only haemoglobinuria, i.e. 
no evident corpuscles. 

Notwithstanding these indications, the cystoscope will frequently 
have to be used to clear up the diagnosis. 

Tubercle bacilli or bits of malignant growth may occur in either, 
and offers no assistance in localising diagnosis. 

If we decide that the blood comes from the kidney, we have the 
following points : — 

From Hilum. From Substance. 

Free haemorrhage Smokiness merely, and casts of renal tubules ; if 
and ureteral casts. haemorrhage is free traumatic history almost 

invariable. 
Often haemoglobinuria only. 



Never haemoglobin 

uria. 
Frequently associ 

ated with pus. 



Practically never with pus, 
being pyaemia. 



the only exception 



As with pus, we must consider the diagnosis of the cause of the 



haemorrhage. 



From urethra, 
vagina, and 
vulva. 

From prostate — 
Carcinoma. 

Abscess. 



Varicose veins. 



Traumatism, carcinoma, etc. ; the parts are so 
open to inspection that nothing further need 
be said. 

Enlargement revealed to examining finger in 

rectum ; chronic history of local pain. 
Tenderness to finger ; possibly a fluctuating 

swelling ; acute history of prostatic trouble ; 

pus with the blood. 
These unquestionably exist on an enlarged 

prostate and at the base of bladder, and may 



1 " Strangury" is a term used to express a pathologically excessive desire to pass 
water, with frequent attempts to fulfil the desire : it is a symptom of excessive irrita- 
tion of kidneys, and probably reflexly of the prostate too. 



vi DISEASES OF THE URINARY ORGANS 205 

give rise to severe haemorrhage ; their presence 
will chiefly be guessed at by the absence of 
other causes ; only the cystoscope can prove 
their presence. 

3. Bladder. The causes of haemorrhage from the bladder are 

the same as those of pus (q.v.) with the excep- 
tion of simple varicose veins, and innocent 
papillomata. In the late stages the diagnosis 
will be self-evident ; in the earlier stages the 
cystoscope or sound is simply and absolutely 
indispensable ; without one or possibly both of 
them diagnosis is impossible. 

4. Kidney. Unless one of the following — heart disease (for 

infarcts), tubercle bacilli, fragments or new 
growth, or tumour in loin — is present, and 
reveals by its presence or by its character the 
nature of the kidney trouble, we may say at 
once that exact diagnosis of the cause of renal 
haemorrhage is impossible without exploration. 
Acute nephritis (with its attendant general 
symptoms), haemophilia, and those cases in 
tfhich only some form of blood pigment (with- 
out corpuscles) is present, are of course ex- 
cepted ; their diagnosis being more from 
general considerations than through the local 
haemorrhage. I have seen very obstinate renal 
haemorrhage follow influenza without anything 
occurring to give any hint of a more definite 
diagnosis. Stone, tubercle, and carcinoma are 
far the most frequent, and must be suspected 
until other cause can be found or definitely 
excluded. 



CASTS 

To mention all casts possibly found in urine it must be stated 
that urethral or ureteral casts may be met with ; they will, however, 
usually be recognisable by the naked eye, and will be simply blood 
clots. They have been sufficiently noticed under Haematuria. 

It remains, therefore, to enumerate the various kinds of renal 
microscopic casts that are met with, and consider their value as 
diagnostic factors. As a convenient method of remembering them, 



2 o6 DIFFERENTIAL DIAGNOSIS chap. 

we may put them down in the order in which they must occur in a 
case of acute nephritis from the stage of congestion onwards. Thus 
we shall have — 

i. Small hyaline casts from simple coagulated serum exuded in 
the early hours of congestion, generally overlooked owing 
to the rapid production of — 

2. Blood casts, which form from the blood escaping into the 

uriniferous tubules in the next stage of the inflammatory 
process ; inflammation rapidly causes the death of renal 
epithelium, and consequently — 

3. Epithelial casts soon follow, formed of masses of rapidly-shed 

epithelium. That which at first remains attached to its 
membrane, but eventually dies, undergoes degeneration, 
and disappears from the tubules as — 

4. Granular casts, — if the cells degenerate so as to lose their out- 

line, and become mere granular detritus, or — 

5. Fatty casts — if, on the other hand, the degeneration takes 

a fatty form ; and certainly in the later stages of nephritis, 
when the acute inflammatory phenomena have subsided, 
fatty casts are more abundant. Lastly — 

6. Large hyaline casts are formed by the coagulation of an ex- 

udation taking place into tubes denuded of their epithelium, 
and consequently with larger calibre. 

Provided that the secretion of urine is fairly free, the relative 
abundance of any of these casts gives a rough estimate of the 
rapidity with which epithelium is dying and being shed. So that 
from a clinical point of view the abundance and the nature of the 
predominant form of cast may be able to give us some idea of the 
progress of the case. Thus blood casts will not be likely to pre- 
dominate in any case that is improving ; fatty casts rather point 
to a want of recuperative power in the kidneys, while a large total 
number of casts of epithelial origin point to a grave destruction of 
renal substance still going on. 

Beyond these hints, casts are of comparatively little value in a 
case of acknowledged and definite nephritis ; but it is in cases of 
less definite character, and more insidious onset, where albuminuria 
first draws serious attention to the renal function that the presence 
of casts is such an important point to determine. Thus, in the 
following conditions more especially (though in no case of albumin- 
uria must repeated searches for casts be omitted), the presence of 
casts must give us serious concern for the safety of our patient. 



vi DISEASES OF THE URINARY ORGANS 207 

1. Pregnancy. 

2. Any abdominal tumour likely to cause pressure on kidneys 

or renal vessels. 

3. Any case in which serious surgical procedures of any kind are 

contemplated. 

4. Convalescence from, or presence of, scarlet fever, diphtheria, 

and in fact any acute illness, especially of microbic origin. 

5. In a case hitherto regarded as functional albuminuria. 

The presence of numerous casts shows that the albuminuria is 
probably due to something more than slight nutritive weakness of 
the kidney, and therefore ceteris paribus adds enormously to the 
gravity of the situation. 

URATES 

It is well to remember that this is the only deposit that occurs 
in urine (which has not decomposed) as the result of simple cooling, 
and hence when the means are not at hand for properly testing the 
secretion, if the urine was bright and clear on voidance, a patient's 
mind can often be set at rest at once by finding that the secretion 
was clear until it cooled. 

We have already noticed that urates are often enough present 
in large quantities in health, under various conditions of exercise 
and weather, etc. Their pathological associations are as numerous 
as the whole nomenclature of diseases, for there is no illness which 
may not be associated with (? actually cause) a deposit of urates in 
the urine. As a matter of practical clinics, therefore, their diag- 
nostic value or importance is not great, but we must generally 
suspect when urates are in excess 

1. Febrile disorders of some kind, especially rheumatism ; or — 

2. Alimentary disturbance, and especially if gout be in question. 

In the former class they probably indicate an insufficiency of 
oxygen to burn up the increased waste products ; in the latter some 
slight disturbance of the course of the body's metabolism ; in either 
case they may be said generally to indicate the necessity for a free 
evacuation of the bowels, and due attention to the organs of 
digestion. 

Their relationship to stone will be briefly referred to under that 
head. 



2o8 DIFFERENTIAL DIAGNOSIS 



OXALATES 

These are comparatively unfrequent elements in a deposit, and 
but little is known of their causation beyond the fact that they may 
occur in quantity after a meal in which rhubarb or sorrel leaves has 
been freely partaken of. A few doses of nitro-hydrochloric acid 
will rapidly remove them from the urine, and the aching pain from 
the back, the latter being their only known symptom. 

PHOSPHATES 

Phosphorus in combination appears in the urine in four groups 
of bodies, viz. — 

i. In combination with organic radicals in the shape of lecithin, 
protagon, etc., the existence of which is well recognised in 
the excretion ; but the results of their estimation and the 
significance of their presence are not yet available for 
ordinary clinical work, and therefore nothing further will 
be said about them. 

2. As the phosphates of the fixed alkalies Na and K. 

3. As the phosphates of the alkaline earths Ca and Mg. 

4. Triple phosphates. 

On these last three groups a word or two may be said. 

(2) Phosphates of Sodium and Potassium. — We have already noted 
these bodies as the chief cause of the acidity of the urine. The only 
other caution connected with them is to remember that they are so 
freely soluble in water that they never in untreated urine form any 
part of the very common phosphatic deposit. This caution is the 
more necessary, as a student almost invariably replies, " Sodium and 
potassium " if asked what phosphates are present in a deposit. 

(3) Phosphates of Ca. and Mg. — These are the phosphates which 
are precipitated on boiling, or in a urine which is acid without 
artificial treatment. So long as they appear only on boiling, or as 
a scarcely appreciable quantity in an otherwise healthy urine, they 
may be neglected in diagnosis ; but when they appear in distinctly 
measureable quantities they assume at once a position of greater 
importance, and a few points will be noticed {vide Phosphatic 
Diabetes). 

(4) Triple Phosphates. — The name "triple," though sanctioned 
by long usage, seems to me somewhat badly chosen, because, unless 



vi DISEASES OF THE URINARY ORGANS 209 

one is very careful to explain the nature of these crystals, students 
jump to the conclusion that triple means that three metals are 
combined with the phosphoric acid instead of understanding that 
all three atoms of hydrogen are replaced, two by the dyad Mg, and 
one by the monad Am, so that the formula is Mg Am PO^ 
and aq. 

The only clinical deduction their presence allows is, " This urine 
has decomposed." 

Why this deduction ? 

Because there is no other available source for the Am except 
that provided by the decomposition of urea. 

Then arises the all-important point, " Did this decomposition 
take place inside or outside the body ? " If outside, and only after 
some time, it represents merely a normal event in the natural history 
of an organic substance exposed to the action of micro-organisms. 
If inside, or within say an hour of being passed, we know at once 
that either the bladder or renal pelvis (or possibly both) is in a very 
unhealthy condition, which, if not speedily improved, is likely to 
lead to most disastrous consequences. 

Very slight attention to the history will usually suffice to clear 
up the point, especially if the question be asked, "Are you sure 
the urine was quite clear on being passed, and only clouded after 
standing some time ? " Earthy phosphates without ammonia, pus, 
and chyle, are the only fallacies in that which is passed cloudy, 
while urates will be the only fallacy in that passed clear, and each 
of these can very readily be differentiated {vide Chemical and Micro- 
scopical Tests). 

We have already (p. 200) discussed the diagnosis of kidney or 
bladder as the seat of the trouble ; and for relief of the symptom 
(not necessarily of the disease) local injections of hot boracic lotion 
and benzoate of ammonia in 15 grain doses are, in my experience, 
the most likely means. 

URIC ACID 

On what may be called the pathology of the uric acid diathesis 
of gout and of gravel and nephrolithiasis, so much has been written, 
so many theories have been propounded, and in their turn con- 
futed, that it seems desirable to state what is accepted as fact, and 
separate it from the more theoretical and disputed points. This 
we may do in parallel columns, so as to draw more pointed attention 
to the arguments. 

p 



DIFFERENTIAL DIAGNOSIS 



Points agreed to by all, and accepted Points about which conflicting theories 
now as facts. and statements are still being made. 

As to Uric Acid itself 



That uric acid is one of the 
possible products of the de- 
composition of the complex 
nitrogenous bodies which 
exist as component parts of 
the various tissues of the 
body, or which are taken into 
the body as food stuffs. 

That it is practically the only 
representative of nitrogenous 
waste products in some ani- 
mals, e.g. birds and snakes. 

That it is present in certain 
small amounts in the urine of 
every healthy human being. 



:ion 



4. That its chemical composit 
is C 5 H 4 N 4 0. J , and thus con- 
tains a less proportion of O 
than urea CH 4 N 2 0. 



Whether the food {i.e. that part of 
it which has not enteied, or will 
not enter into the molecular 
constitution of the body tissues) 
or the tissues is the ultimate 
source of the uric acid found in 
the urine of man. 

Whether the urates of snakes' 
urine, etc., are identical in 
nature, as well as composition, 
with those of human urine. 

Whether it should bear any con- 
stant proportion to the urea, and 
how to account for the varying 
amounts and proportions found. 

Its exact chemical relationship to 
urea, i.e. whether in the human 
body urea can be, and is made 
from uric acid, or vice versa ; 
or whether they appear side by 
side, as it were, as independent 
results of the same chemical 
processes of decomposition ; or 
whether each requires a separate 
series of reactions for its pro- 
duction. 



As to Locality of M^anufacture 



5. That it is manufactured some- 

where in the body. 

6. That it exists in the blood of a 

patient who has gout. 



Whether in the liver, the tissues 
generally, the blood, the spleen, 
or the kidney. 

Whether it exists in the blood of a 
healthy individual. 



As to its Clinical Relatio?iships 



7. That there are two well-marked 
clinical types of trouble asso- 



Whether these two diseases must be 
reckoned as primary renal affec- 



DISEASES OF THE URINARY ORGANS 



Points agreed to by all, and accepted 
now as facts. 

dated with uric acid, and 
that these two, viz. gout and 
gravel, may and do occur 
separately. 

8. That heredity plays a strong 

hand in the production of 
gout or gravel, but frequently 
alternations of the two in 
successive generations are 
met with. 

9. That cartilage and fibrous 

tissue do become infiltrated 
with crystals of urate of 
sodium. 



10. That per pound of body 
weight children excrete more 
uric acid than adults. 

11.* That gout is as rare in chil- 
dren, compared with adults, 
as stone and gravel are 
common. 

12. That gout, lead poisoning, 

and cirrhotic kidney occur 
in the relationship of pre- 
disponent, excitant, and re- 
sultant in a far larger pro- 
portion than mere coincidence 
will account for. 

13. That diet can influence gout 

and gravel. 



Points about which conflicting theories 
and statements are still being made. 

tions, or whether the kidney 
suffers only secondarily. 



Whether heredity or personal en- 
vironment (in its widest sense) 
is the stronger factor. 



Whether this deposition of urate 
causes the painful affection of 
a given joint ; 

Whether such deposits can be re- 
absorbed ; 

Whether so-called acute gouty arth- 
ritis is not really acute neuritis ; 

Whether the deposition is a cause 
or consequence of local necrosis. 

Whether this indicates freer ex- 
cretion only, or more active 
formation ; in fact, its meaning. 

The essential meaning of this. 



Which of the three is predisponent, 
excitant, or resultant ; and 
whether each one may not act 
in any capacity at times. 



Precisely what kind of diet is best 
for gouty patients. 



In conclusion, we may say that until some of these points are 
authoritatively settled by a unanimous agreement, above all, the 
tissue source, and seat of manufactory of uric acid, the only 
practical clinical points that may be safely deduced are : — 



That uric acid, by its presence in the body in excess, is 



2i2 DIFFERENTIAL DIAGNOSIS chap. 

capable of working mischief, or at least that uric acid is the outward 
and visible sign of a vital metabolism which is incompatible with 
perfect health. 

2. That if we find it in excess in the urine or body, we should 
recognise its potency for evil, and try by some means to check its 
production in, or ingestion into, the body. 

3. That as regards diet, exercise, and even drugs, each case 
must be treated at first more or less experimentally, and later by 
the light of such knowledge as experience of the individual case 
may give. Sodium salicylate and iodide, with moderation in 
butcher's meat and alcohol, are the most promising measures with 
which to commence to treat an unknown patient. 



GLYCOSURIA 

With regard to sugar in the urine, we are in a very similar 
position to that in which we stand in the case of uric acid. Many 
facts require explanation, and many theories have been brought 
forward in consequence. Were it not for the resolute opposition of 
Dr. Pavy, who has made diabetes the special object of a life-long 
study, we might say that there is complete unanimity in the views 
of the morbid physiology of glycosuria. A similar arrangement to 
that we adopted in the case of uric acid will again serve to empha- 
sise fact and theory. 

Fact. Theory or Doubt. 

1. That sugar does occur in patho- Whether minute traces of sugar 

logical quantities in the urine. are or are not normal in the 

urine. 

2. That pathological condition may Whether glycosuria and diabetes 

be — ■ can be separated as two distinct 

(a) Temporary, as after chloro- conditions ; and supposing they 
form and experiment. can, what is the real and precise 

(b) Intermittent, as in some relationship between the glyco- 
elderly patients. suria of diabetes and the remain- 

(c) Permanent till death, as in ing characteristic symptoms of 
many cases of diabetes in that disease. 

both young and old. 

3. That in many cases, especially 

of Groups (a) and (6), it is 
present without the usual as- 
sociated symptoms of actual 
diabetes ever occurring ; but 



DISEASES OF THE URINARY ORGANS 



213 



Fact, 
in many commencing as appar- 
ently simple glycosuria the 
more severe symptoms do 
eventually occur. 

That diet, especially with regard 
to carbohydrate material, does 
influence very markedly almost 
every case of glycosuria. 

That the liver contains glycogen 
during life ; that this glycogen 
is derived mainly from carbo- 
hydrate food material ; that 
after death, if no precautions 
are taken, the liver can and 
will convert nearly all the 
glycogen into sugar. 



6. That in many cases the liver is 
in some way the main seat of 
those disturbances in metabol- 
ism which result in glycosuria 
and diabetes. 



Theory or Doubt. 



What is the precise connection 
between food and sugar in the 
urine. 

It is on this point that Dr. Pavy is 
especially insistent, viz. that we 
have no proof that what the 
liver does after death it is cap- 
able of doing during life ; and 
hence he denies the more com- 
monly accepted view, viz. that 
the liver seizes upon all carbo- 
hydrate material, converts it into 
glycogen, and then reconverts it 
into sugar, according to the 
needs of the body. 

The real nature of the disturbance, 
whether it is — 

(a) Merely excessive escape due 
to excessive circulation through 
the blood vessels. 

(b) Excessive escape due to 
excessive action of the cells of 
the liver. 

(c) Faulty metabolism of the 
cells, so that a wrong sort of 
sugar is produced, useless for 
the tissues. 

(d) Faulty metabolism in not 
seizing the sugar brought to the 
liver and converting it into 
glycogen. 



As regards Morbid Anatomy 



That in some cases of diabetes 
the pancreas is found diseased. 



Whether the disease of pancreas 
means a fifth view of the morbid 
physiology of diabetes, equivalent 
to a diminished destruction of 



2i 4 DIFFERENTIAL DIAGNOSIS chap. 

Fact. Theory or Doubt. 

sugar by the internal secretion 
of the pancreas. 

8. That in the great majority of Whether there are not such micro- 

cases of diabetes no naked-eye scopical changes in the medulla 

appearances are found capable as might explain altered meta- 

of explaining the causation of bolic power on the part of the 

the trouble. liver 

9. That the coma from which the The precise nature of the substance 

great majority of diabetics die which, by its presence in the 

receives no adequate post- blood, causes the coma, 
mortem explanation. 

In conclusion, whatever views may be held on the disputed 
points in the pathology of diabetes, the diagnostic points are very 
simple, for the facts are so strong that no objection can be raised 
to the statement, " If sugar be constantly present in the urine — for 
a longer period than, say, twenty-four hours — in sufficient quantity 
to be detected by thirty seconds' boiling with Fehling's solution, 
there is a serious pathological condition present which requires the 
careful attention of the medical man." (For one or two further 
remarks of a clinical character, vide Diabetes.) 



URAEMIA 

This term was originally invented to express a series of symp- 
toms due to a supposed excess of urea in the blood ; we now use 
it in a wider sense, or rather in a different sense, to cover the 
symptoms produced by the retention within the blood (or tissues) 
of waste products in general, which should be eliminated with the 
urine. Thus far everyone is agreed, but when the further question is 
put — "What is, or are, the particular waste products ?" — no answer is 
forthcoming except negative ones. It is not urea, nor uric acid, nor 
potassium * {vide footnote), nor water, nor inorganic salts, nor kreatin, 
in fact, it is not any single ingredient of the urine which has 
hitherto been isolated. 2 

The nearest probability would be a suggestion that each organ 
and tissue is responsible for its own share in the production of the 
total phenomenon ; the special waste products of each (whatever 

1 The latest view of all is that uraemia is due to retention of potassium salts. 

2 All these points are conclusively proved by M. Bouchard's work on auto- 
intoxication, translated by Oliver. 



vi DISEASES OF THE URINARY ORGANS 215 

their nature) acting as a hindrance to the proper functioning 
of itself (and probably to a varying extent of other organs). 

Diagnosis of Uraemia 

To associate its occurrence into the following groups will, I think, 
best conduce to its diagnosis. 

Group A. — Acute and severe, probably, though not certainly^ 
producing a rapidly fatal termination to — 

(1) A known and watched case of kidney disease. 

(2) A known and watched case of other disease in which 
urinary symptoms are now, or have been all along, pro- 
minent, e.g. cardiac disease with suppression. 

(3) An unknown and unwatched case of sudden illness 
of convulsive or comatose type in a patient previously sup- 
posed to be in good health. 

Group B. — So-called chronic uraemia, in which the symptoms, 
though possibly acute enough and severe enough in them- 
selves, pass off or yield to appropriate treatment, and 
recur again and again over months or, it may be, years. 

Of Group A, Nos. (1) and (2), I have nothing to say beyond 
what will be found in every text-book. The symptoms are fairly 
uniform, starting with a violent headache or sudden blindness, or 
acute vomiting, or diarrhoea, and rapidly passing into convulsions, 
coma, and death ; or it may be sudden convulsions or coma, passing 
into death. In any case, the only difficulty in diagnosis rests in 
bearing in mind the great possibility, or rather probability, of uraemia 
supervening in a certain class of diseases. 

Group A, No. (3), presents great difficulty in diagnosis, but as 
the condition is one presenting great likeness to alcoholic and other 
poisoning and cerebral disease, it is fully discussed under the 
heading with which the lay press has made us unhappily familiar, 
viz. " Drunk or Dying " (q.v. Chap. IX.). 

Group B is the group of chronic uraemias to which I wish to 
draw special attention, as I feel convinced that many cases of it 
pass unnoticed or called by another name, for the simple reason 
that students are so accustomed to the idea of the acute, rapidly- 
fatal symptoms as the only form of uraemia, that they overlook the 
" fringes " (to borrow Dr. Goodhart's phrase) of the condition. 

The late Sir Andrew Clark, I believe it was, who coined the 
expression "renal inadequacy," and this is the condition which 



216 DIFFERENTIAL DIAGNOSIS chap. 

underlies and explains many or all of the following symptoms so 
commonly found in elderly, and even young people, whose urine is 
habitually only just within the physiological limits of the product 
quantity x specific gravity. I refer to attacks of indigestion or 
diarrhoea without obvious dietetic irregularities, to attacks of deaf- 
ness, giddiness, etc., swimming in the head, so often thought of as 
precursors of apoplexy ; to severe headaches of a prostrating char- 
acter, to transitory paresthesia;, felt in parts of the body or limbs, 
or pareses of the same parts ; to a frequent feeling of malaise and 
general despondency ; nay, I will go farther and say, without fear 
of contradiction, that this same renal inadequacy is at the bottom 
of the known experience that operations on kidney subjects do 
badly, that it explains the liability of many patients to chronic 
bronchitis and emphysema, pneumonia, pleurisy, pericarditis, peri- 
tonitis (whether serous or suppurative), cardiac failure ; that, in fact, 
it is the real meaning of those so-called intercurrent affections, not 
excluding acute nephritis, which so frequently close the scene in 
cirrhotic kidney. It is the circulation of imperfectly depurated 
blood that renders all these organs so liable to break down with 
acute inflammatory mischief. This persistent and steady, though 
it may be very slow, accumulation of waste material is as essenti- 
ally chronic uraemia as is the rapid accumulation acute uraemia. 

As far then as diagnosis is concerned, the rule may be emphatic- 
ally laid down that in all diseases of the above character the urine 
should be systematically examined every day, and especially is this 
necessary if the patient is over forty. An elaborate analysis is not 
required, but the total quantity and specific gravity are essential for 
a correct appreciation of the output of waste organic material. 

Suppression v. Retention 

If there is reliable information that very little or no urine has 
been passed, say for twenty-four hours, these two conditions cannot 
easily be confused. An abdominal examination must be made : this 
will or will not reveal the presence of the distended bladder ; in either 
case, the catheter must then be passed to relieve the symptom if 
the bladder be distended, or to prove the absence of urine. The 
only exceptions to the whole of the above rule and treatment are 
occasional cases of pure hysteria, in which the pleasures of instru- 
mentation overcome the discomforts of a full bladder. Such cases 
require great tact in handling, but offer no diagnostic difficulties. 

Difficulties in diagnosing retention may occur when overflow is 



vi DISEASES OF THE URINARY ORGANS 217 

also present, or when micturition is alleged to be natural. The 
former occurs commonly enough in puerperal cases (I have known 
a distended bladder under these circumstances called acute 
metritis), and should also always be held in mind when diseases of 
cord and brain are being treated. It will, of course, be usually 
associated with local pain, directing attention to the bladder, but if 
unnatural anaesthesia be present, a distended bladder requires to be 
borne in mind and looked for. The latter condition, i.e. disten- 
sion, with alleged natural micturition, is practically confined to 
elderly male patients with prostatic trouble. It is apt to be very 
misleading, owing to the gradual acquirement of a condition of 
tolerance for increasing quantities of residual urine. I have seen 
a patient with bladder distended to the umbilicus who assured me 
that he could not pass me any water because he had micturated 
just before his visit. He was totally unconscious of his urinary 
condition, which proved fatal within a few weeks. 

The causes of suppression of urine, i.e. of anuria with empty 
bladder, may thus be tabulated : — 

A. Mechanical Stone {vide Stone in Kidney). 

blocking of Carcinoma, — previous haemorrhage, and tumour, 
ureter, due to Tubercle, — previous pus, and haemorrhage. 
Blood clot, — previous haemorrhage. 

B. So - called func- Heart failure, or other form of venous back pres- 

tional from sure, — cardiac bruits, with obvious back pres- 

kidney condi- sure, or swelling and tumour of abdomen, 

tions, due to Active irritation, such as that caused by drugs, — 

history of taking a drug. 
Actual inflammation, — other signs of acute neph- 
ritis, anaemia, puffmess of eyelids, etc. 

The causes of retention, i.e. anuria, with a full bladder, are 
again : — 

A. Mechanical ob- Position diagnosed by the catheter ; uterine con- 

struction, dition also to be thought of. 

B. Functional inca- Cause to be sought in the nervous system, or in 

pacity of ex- previous history of over-distension. 



pulsion. 



BRIGHT'S DISEASE 



Before saying anything as to the diagnosis of the various forms 
of Bright's disease, it would be well to define the term. There are 



218 DIFFERENTIAL DIAGNOSIS chap. 

then four fairly well-marked types of it from a clinical point of 
view : — 

i. Acute Nephritis. — The word "acute " as used in medicine sadly 
needs accurate definition : sometimes it has mainly refer- 
ence to time, i.e. with well-marked definite onset, without 
reference to the severity of the symptoms ; sometimes it 
is used to denote more the intensity of the symptoms, i.e. 
in our present illustration the smoky or bloody urine. 
Acute nephritis is practically always due to a toxaemia, i.e. 
to the efforts of the kidney to secrete from the blood some 
substance which actively irritates the kidney cells in the 
process of separation, e.g. the poison of scarlet fever, diph- 
theria, or substances produced in the blood by a condition 
popularly known as a chill. 

2. Consecutive Nephritis. — This is a convenient term to desig- 

nate the condition of a patient who has (a) at some pre- 
vious period suffered from acute nephritis, and has never 
since been quite free from urinary changes ; (b) has drifted 
into a condition of renal disease without marked onset, as 
in some of the scarlet fever cases not under careful obser- 
vation, and (?) some cases of earlier albuminuria simplex 
{q.v.); or (c) has his kidneys irritated by local conditions, 
such as stone, simple blocking or kinking of the ureter, and 
all forms of surgical kidney. The group is obviously a 
mixed one, and most of the cases will in practice naturally 
have a specific name applied to them, but they all have 
one point in common, that if they last long enough, and if 
the essential kidney structure does not wholly disappear, 
they lead eventually to the form of granular kidney known 
as the small white or secondarily contracted kidney. 

3. The Cirrhotic Kidney, of which one type is the later stages of 

Group 2, and the other is the small, red, granular kidney 
so frequently associated with degenerate vessels and large 
heart, with age over forty, with gout, and with lead poison- 
ing. It must be ever constantly borne in mind that either 
type may at any moment blaze up into an acute nephritis ; 
in fact, this is the commonest event in their course. 

4. Large White Kidney. — A disease just as much sui generis and 

absolutely independent of other kidney trouble, as is, say, 
typhoid fever or cerebral glioma. It has a rapid history, 
with an invariably fatal termination within three to six 



vi DISEASES OF THE URINARY ORGANS 219 

months. It never starts from, or turns into anything else, 
and may be called acute degeneration (fatty changes pre- 
ponderating) of the kidneys. 

As to their clinical course and main danger signals, these four 
types may be briefly epitomised as follows : — 

Acute Nephritis threatens life chiefly in its early days, and that 
almost entirely by suppression and acute uraemia. If this 
stage be passed, we may then say that the lapse of nine to 
twelve months will show whether the case will end in 
complete recovery or will drift into one of consecutive 
nephritis. 

Consecutive Nephritis. — Of the sub-groups (a) and {b) the dura- 
tion is commonly one of years, though of course often much 
less, in which the patient shows important and marked 
changes in the urine (albumen and casts). The main 
clinical features of the condition will be occasional puffiness 
of the face, especially in the lower eyelid, general flabbiness 
and malaise, and, above all, anaemia, to which I would draw 
special attention as the main element in the disease. So 
long as the patient keeps a fair colour, or the anaemia does 
not advance, so long are there good hopes of prolonging 
life ; but with the advance of blood impoverishment must 
come increased anxiety as to the advent of severe uraemic 
symptoms, of which the anaemia is the advance guard and 
warning beacon. Of the sub-group (c) the dangers are 
much the same, for they essentially depend upon disorgan- 
isation of the kidney, but the prognosis has two elements in 
it — first, " How far has the destruction of the kidney sub- 
stance progressed before surgical measures are adopted?" and, 
secondly, " Is the primary cause of the trouble one which can 
be permanently cured by these surgical measures if they are 
applied ? " 

Cirrhotic Kidney. — The first group is sufficiently sketched under 
Consecutive Nephritis, of which, indeed, it forms merely 
the concluding chapters. The other type of cirrhotic kidney, 
i.e. the independent form without previous history of urinary 
trouble, can scarcely be said to have a clinical course. It 
begins so insidiously that it hardly comes under notice until 
the thickened arteries and the hypertrophied (probably also 
dilating, vide Morbus Cordis) heart are discovered on the 
routine examination of a patient who comes before us struck 



2 2o DIFFERENTIAL DIAGNOSIS chap. 

down by apoplexy, or affected with one of the diseases 
already mentioned as essentially uraemic {q.v.) in nature. 
The last scene is always either of this nature, or else a simple 
uncomplicated uraemia, which in turn is brought about either 
by an absolutely too great organic destruction of kidney 
tissue, or by an acute nephritis, which renders a still organi- 
cally adequate kidney functionally inadequate. 
Large White Kidney. — This has for years been described as a 
form of chronic Bright's disease, and included amongst those 
cases for which I have adopted the term Consecutive Ne- 
phritis. A comparison of the accounts of writers thus 
describing it, combined with my own post-mortem ex- 
perience, have compelled me to claim for it a course which 
is, at any rate, acute enough when measured by time, and 
also by urinary symptoms. If at the post-mortem the 
kidneys (not being amyloid) are very white, large (say to- 
gether over 14 ozs.), and especially if the capsule strips 
easily without tearing the substance at all, but leaving a 
perfectly smooth surface to the organ, then the clinical 
history shows only a four to six months' duration of illness 
at the outside, and frequently one of only six to ten weeks. 
The main features of the illness are always the same, viz. 
very marked anaemia, excessive oedema, especially of thighs 
and legs (large white legs, large white kidney, is a patho- 
logical proverb), and a urine such as is tabulated below ; 
and these serve to distinguish this affection during life from 
any other except the absolutely final chapter of a con- 
secutive nephritis which, if diagnosis is required, can be 
readily recognised by its commencement. The invariable 
ending of large white kidney is acute uraemia. 

This brief sketch shows plainly enough that all forms of Bright's 
disease have a distinct tendency to drift into serious uraemia, the 
only exception being some cases in Group (c) of Consecutive or 
Secondary Nephritis, provided that the local cause of the nephritis 
is one which is capable of complete removal by surgical aid, and 
also provided that the condition is ascertained and removed before 
extensive, serious, and progressive destruction of renal tissue has 
been set up. Our first object, then, when a patient presents himself 
with a condition of urine indicating damage to the kidney, is to 
ascertain whether such a removable cause is present or not. This 
will, however, be more conveniently discussed in the next section ; 



DISEASES OF THE URINARY ORGANS 



in the present one we will discuss the diagnosis of the uncompli- 
cated forms of Bright's disease. 

A slight inquiry into the previous health and urinary history of 
the patient, combined with a knowledge of the onset of the present 
illness, will speedily separate — 



Primary acute nephritis "| 

Secondary acute nephritis (as an I on the one 
incident in chronic) j hand from 

Large white kidney J 



Simple chronic nephritis 
of either type without 
the acute exacerba- 
tion. 

They will also separate very distinctly the primary from the 
secondary acute nephritis. The profound anaemia of very rapid 
onset, combined with the extreme oedema, are usually striking 
enough to separate large white kidney from either form of acute 
nephritis. Should these general indications not be sufficient, the 
condition of the urine tabulated below will settle the matter. In 
the more chronic conditions a keen eye to note progressive asthenia 
and anaemia, and a careful analysis of the urine from day to day for 
a short period, are the important requisites for estimating the stage 
which the sufferer has reached on his road to uraemia. 



Urine in Bright's Disease (and in Lardaceous Kidney) 

Large White. 



Acute. 
Quantity — 
Much dimin- 
ished, some- 
times to sup- 
pression. 



Blood— 
Invariably pre- 
sent in visible 
amount; 
smoky or 
bloody. 
Sfi. Gravity — 
Increased. 



Consecutive and 
Cirrhotic. 1 



Increasing in 
proportion to 
the change 
towards cir- 
rhosis ; di- 
minishing at 
the last. 

Absent without 
acute exacer- 
bation. 



Much dimin- 
ished, but not 
to suppres- 
sion. 



Only detected 
by the micro- 
scope. 



Diminished, 
even if quan- 
tity diminished. 



Probably below 
average. 



Lardaceous. 

Usually in- 
creased, but 
not always. 



Absent. 



About normal. 



1 These changes are independent of pus, blood, crystals, etc. , produced by any 
possible local trouble, and refer to the nephritis only. 



DIFFERENTIAL DIAGNOSIS 



Acute. 

Albwnen — • 
Much, often 
nearly solid, 
probably col- 
our ed by 
blood. 



Casts — 
Blood, epithel- 
ial, etc. {vide 
under Casts). 



Colour — 
Dark, concen- 
trated, smoky, 
or red. 



Consecutive and 
Cirrhotic. 



Large White. 



Variable, but From half to 



solid, always 
much, not 
coloured by 
blood. 



generally not 
more than a 
trace unless 
serious con- 
dition coming 
on, often quite 
absent. 



Very few, hyaline Plentiful, some 

or fatty, more epithelial, but 

numerous if mostly fatty 

acute exacer- and hyaline, 
bation. 



Very light, ex- 
cept in acute 
exacerbation. 



Natural. 



Lardaceous. 

Variable, but 
always con- 
siderable, i.e. 
one - fifth or 
more. 



Sometimes 
none, may be 
many, and 
are said some- 
times to show 
lar daceous 
changes. 

Usually lighter 
than natural. 



In the daily analysis the points of especial importance are the 
total quantity and the specific gravity, the relative abundance of 
casts and other debris. The former giving us the product of 
specific gravity by quantity, which is a rough indication of the 
output of waste material ; the latter giving a fair estimate of the 
activity of renal destruction. In comparison with these two in- 
dications the amount of albumen sinks into insignificance. 

We may now discuss those conditions of the urinary tract which 
are liable to cause by their continuance a consecutive or secondary 
nephritis, or to be mistaken for Bright's disease owing to certain 
urinary changes produced by them. They may be enumerated as 
follows : — 



Group I. Preputial or urethral stricture, prostatic enlargement or 
other affection of the prostate, stone in the bladder, etc., 
in fact, peripheral obstacles to the escape of urine 
from the bladder, as well as certain ulcers and growths 
of the bladder itself. 

Group 2. Similar affections of the ureter arising in its structure, or 
affecting it from without. 



vi DISEASES OF THE URINARY ORGANS 223 

Group 3. Affections of the pelvis or substance of the kidney — 

Stone. Hydronephrosis from un- 
Tubercle. known causes. 

Malignant growths. Hydatids and other rarer 
Undue mobility. affections. 

The differential diagnosis of the members of Group 1 is essenti- 
ally surgical, and does not ordinarily present much difficulty, as the 
prepuce, penis, urethra, prostate, and bladder are open to direct 
examination and investigation by the eye, finger, bougie, and cysto- 
scope. From the urgency of their symptoms they compel surgical 
interference, whatever be the functional capacity of the kidneys as 
a factor in prognosis, so that the possibly associated Bright's disease 
may be temporarily left out of the question. 

The presence of a member of Group 2 can only be surmised 
by the positive fact of the presence of pathological urine, or a 
tumour in the abdomen, combined with the negative fact of the 
absence of disease from the bladder down to the prepuce, leaving 
us to infer that the trouble is situated in ureter or kidney. The 
only cases in which, then, the ureter would be suspected would be 
the disappearance of a known collection of pus with profuse pyuria 
appearing, or the discovery of a hydronephrotic tumour. In practice, 
however, it is impossible to distinguish even these cases from 
trouble at the hilum of the kidney. 

The third group, viz. affection of the pelvis or substance of the 
kidney itself, requires more detailed examination ; and we may 
commence with the three more ordinary affections, viz. stone, 
tubercle, and malignant disease. Though not absolutely germane 
to the subject of differential diagnosis, there is one clinical fact 
that, on account of its tremendous importance, cannot be omitted, 
viz. that any one of these three may — and not as a mere pathological 
curiosity, but even with some little frequency — be present without 
causing either a pathological condition of the urine, or a tumour in 
the abdomen ; not only so, but the patient may even die of obscure 
symptoms, probably urasmic in nature, without the kidney being 
suspected, until a post-mortem examination reveals the most exten- 
sive destruction of one organ, or even of both of them. 

We are, however, now assuming that some or all of the following 
local indications are present — blood, pus, albumen, casts, and other 
deposits in the urine, pain, either colicky or persistent, tumour in 
the abdomen; and we have to consider, from their various com- 
binations, which is the most likely lesion present : — 



224 



DIFFERENTIAL DIAGNOSIS 



The following table shows the chief diagnostic indications : — 



Quantity of 
urine. 



Blood. 



Pus. 



Albumen. 



Other de- 
posit. 



Pain. 



Stone. 

During colic often 
suppre s s ed, 
otherwise un- 
altered or in- 
creased. 

Moderately fre- 
quent, but usu- 
ally not severe, 
and quite inter- 
mittent. 



Not common in 
any quantity, 
unless urine is 
alkaline and 
ammoniacal. 



Unless associated 
with either 
blood or pus is 
really an indi- 
cat ion of 
Bright's, and, 
as such, has 
much impor- 
tance. 

Uric acid, if any, 
and minute 
stones. 

Often none; some- 
times a con- 
stant dull ache, 
but renal colic 
the typical 
form ; active 
jolting almost 



Tubercle. Carcinoma. 

Usually unaltered, Also usually un- 
if any effect it altered, 
is diminished. 



Often a smart 
haemorrhage, 
less frequently 
repeated than 
in other con- 
ditions. 



Often very pro- 
fuse indeed, and 
that with quite 
acid urine, and 
without neces- 
sarily severe 
symptoms. 

Practically only 
in proportion 
to pus. 



Tubercle bacilli 
in the pus. 



Dull ache most 
usually, if any 
at all, but ordi- 
nary attacks of 
colic not un- 
known. 



Haemorrhage not 
infrequent, but 
more likely to 
be a continual 
oozing, there- 
for e blood 
pretty con- 
stantly present. 

Not profuse as a 
rule ; if present 
in quantity, 
severe features 
are usually pre- 
sent. 

In proportion to 
pus and blood, 
and possibly 
some nephritis, 
but obviously of 
no real import. 



Fragments of 
growth possi- 
bly, but they 
are rare. 

Dull ache or 
acute local 
pain ; typical 
colic very rare. 



DISEASES OF THE URINARY ORGANS 



225 



Tumour. 



Stone. 

invariably 
causes exacer- 
bation. 
Of stone per se 
never present, 
but may be a 
hydronephro- 
sis. 



Tubercle. 



Kidney often 
large, may be 
felt as a tumour; 
kidney fre- 
quently hydro- 
nephrotic. 



Carcinoma. 



Tumour if felt 
more irregular, 
much less like 
a kidney in 
shape ; may 
bulge into loin. 



This table will well bear a few clinical remarks. The most 
important practical general statement, and the one most humiliating 
to medical science, is, that after all points have been fully con- 
sidered, the diagnosis will sometimes still remain in doubt ; gravel, 
bacilli, and fragments of growth, the three almost pathognomonic 
signs, may each and all fail us, and we have to call to our aid 
exploratory surgery for the relief of symptoms serious in themselves, 
but of unknown causation. 

Apart from these doubtful cases of impossible separation, we 
may say a few words on the individual conditions. 



Stone in the Kidney 



It has already been mentioned that the kidney may be entirely 
disorganised by stone, without its presence being suspected from 
any active phenomena ; but we are now dealing with an analysis of 
actual symptoms, amongst which renal colic (intermittent in type, 
made worse by jolting movements, passing to the testicle) and 
intermittent hematuria (almost constantly associated with colic) 
are the two most suggestive. It is worth bearing in mind (in the 
presence of colic with suppression of urine) that in a first attack of 
colic from renal calculus both ureters are never blocked at the same 
time, and we therefore have strong hope under such circumstances 
of a first attack that the flow of urine will be re-established within 
a short time, even if the stone be not passed ; but if the patient be 
suffering from an attack of renal colic, and there be a history of 
similar previous trouble, especially if of great severity, then the 
probability of both ureters being blocked is considerably increased, 
and our anxiety for early mechanical relief proportionately acute. 
This is especially the case when we remember that uraemia from 

Q 



226 DIFFERENTIAL DIAGNOSIS chap. 

obstructed ureters is very insidious — a little increased general 
weakness in the patient, an occasional twitch in one or two muscles, 
no obvious ingravescence of these till quite suddenly drowsiness 
and fatal coma set in. 

Tuberculosis of Kidney 

This is most commonly a secondary affection, or rather it would 
be more accurate to say the kidney — if tubercular — is rarely the 
only tubercular focus in the body. 

i. It may be part of a miliary attack, in which case it will only 
be recognised on post-mortem examination ; it possesses no clinical 
diagnostic interest. 

2. It may be associated with obvious tubercle of the lung. 
Here it will be recognised, if at all, by aching pain in the loins and 
urinary alterations — albuminuria, hematuria, or pyuria {q.v.). In 
such a case its recognition is more important from a prognostic 
than from any other point of view, for advanced phthisis is a 
strong contra-indication to any serious operative interference, and 
I have never seen cured, as opposed to merely quiescent, tubercle 
of the kidney. 

3. Even when confined to the genito-urinary tract, the kidney 
may be only secondarily implicated by extension from the bladder. 
Here, frequent micturition, pain in penis, and pyuria will have 
attracted attention, and the cystoscope will have assured us that the 
bladder at any rate is implicated ; renal casts and cells found by the 
microscope, and a continuance of pyuria after the bladder trouble 
has healed, will be the chief indications that the kidney itself is 
also implicated. Lastly, should the case be one of genuine primary 
tuberculosis of the kidney, the diagnosis will be formed somewhat as 
follows : an aching or even an acute pain in the loin will have led 
the patient to seek for advice ; inquiry will then be specially made 
into the urinary function ; or, failing any special complaint, the 
routine examination of the urine will have led us in the same 
direction, viz. to suspect the kidney. Inquiry and examination will 
then have revealed some features of great probability in diagnosis 
— pain, tenderness, hematuria, pyuria, etc. Lastly, to complete 
the diagnosis, bacteriological examination of the urine, or its 
deposit, will frequently enough be necessary, and in suspicious cases 
cannot be omitted. 

N.B. — One ureter may be completely blocked by causation, so 
that the urine may be natural in quality, and possibly also in 



vi DISEASES OF THE URINARY ORGANS 227 

quantity ; hence we must not too hastily acquit the kidney if the 
previous history or local indications point strongly in that direction. 



Malignant Disease of Kidney 

Like neoplasms elsewhere, may be primary or secondary. If the 
latter, diagnosis is very much a matter of indifference in clinical 
work ; the points are identical with those of a primary case, clarified 
considerably by the presence of the original growth. Primary 
malignant disease — sarcomata are tolerably common in children — 
can only be recognised by a process of exclusion ; the haematuria, 
which is far and away the commonest symptom, being common to 
at least three renal affections, whose differential diagnosis has been 
considered above. Unless, then, we can find a tumour in the 
loin or abdomen, or at least some gross irregularity in the outline 
of the kidney, stone and tubercle must be first excluded. The 
cystoscope may show that the blood comes from one ureter only — 
a suspicious circumstance in doubtful cases, for it almost certainly 
excludes blood conditions, and thus renders local disease of some 
description almost certain. 



PHOSPHATIC DIABETES 

Is too rare a disease, at any rate in well-marked form, to require 
any prolonged discussion here, but I mention it to emphasise the 
one essential point in its diagnosis, viz. that the phosphates must 
appear in the urine without any treatment of the fluid — heat, 
alkalies, etc. — and in the absence of decomposition. In a typical 
case they will form a deposit equal to one-quarter, or even one-half 
the bulk of the fluid. The patient will have few or no complaints 
to make except of general flabbiness, langour, and want of energy. 
Routine examination of the urine will complete the diagnosis so 
far as we can at present go. 



DIABETES INSIPIDUS 

Precisely the same remarks apply to this trouble. It is a rare 
disease, of practically unknown causation, and needs only mention 
to emphasise the caution not to call mere temporary polyuria by 
the ominous — to the laity — name of diabetes. The essential point 



228 DIFFERENTIAL DIAGNOSIS chap, vi 

is that, without rhyme or reason — occasionally a blow or shock 
causes it — an otherwise healthy person shall somewhat suddenly 
begin and continue to pass enormous quantities, from 200 ozs. 
upwards, of very light urine with a very low specific gravity — 1002- 
1005 — and no abnormal constituents. This, and a corresponding 
thirst, are the only real diagnostic elements. 



CHAPTER VII 

AFFECTIONS OF JOINTS 

The symptoms and physical signs of a joint trouble are, with one, 
or possibly two exceptions, viz. hysterical knee and the pain in the 
knee when the hip is the seat of disease, sufficiently obtrusive to 
leave no room for diagnostic difficulty in deciding which joint is 
affected ; but the precise structures attacked, and the extent to 
which they are likely to be disorganised or destroyed, with the con- 
sequent future utility of the articulation, will commonly, and speak- 
ing in general terms, largely depend upon the third step in diag- 
nosis, viz. the exact etiological factor at work. Treatment, too, will 
very much depend upon the same factor for its nature and degree 
of activity. Compare the almost passive expectancy of the local treat- 
ment of the joints in simple rheumatic fever with the urgent necessity 
for evacuating a joint full of pus. Thus, both for prognosis and 
for treatment, exact diagnosis is of immense importance. 

The affections, the diagnosis of which I propose briefly to dis- 
cuss, are : — 

Charcot's osteoarthropathy of tabes Rheumatic gout. 

dorsalis. 

Flat foot. Rheumatoid arthritis. 

Gout. Synovitis acute. 
Gonorrhceal rheumatism. ,, chronic. 

Hysterical joint troubles. Tubercle of joints. 

Rheumatism. Traumatism. 

Some of them require only to be borne in mind for diagnosis to 
be at once evident, while in other cases a precise determination of 
the factors at work will remain in doubt after all tests have been 



2 3 o DIFFERENTIAL DIAGNOSIS chap. 

applied. We will commence with an analysis of the symptoms and 
physical signs as the simplest introduction to exact diagnosis. 

A patient who has, or thinks he has, disease in or of a joint will 
come before us complaining of one or more of the following 
symptoms : pain (spontaneous, or on attempted movement), stiff- 
ness, grating, swelling, heat, or redness. 

Pain. — This is a feature common to all cases, with one excep- 
tion, viz. Charcot's joint, which is almost invariably (but not quite 
without exceptions) a painless trouble. The curiously misplaced 
reference of pain to the knee (through the obturator nerve), when 
the hip is the seat of serious trouble, must not be overlooked ; the 
apparent shortening — tilt of pelvis— and physical examination of hip 
will usually clear up difficulties when nothing is found in the knee. 
For the rest the character and severity of the pain give us a strong 
guide to the acuteness or chronicity of the joint trouble. Thus, in 
acute gout, or a pyaemic joint, the pain is sudden in onset and 
agonising in its character. In rheumatism it is usually not so in- 
tense, but more wearying — a constant dull ache. When the bones 
are affected the pain is much worse at night, with jumping and 
starting of the limb on falling asleep. In more chronic affections, 
such as chronic synovitis, rheumatoid arthritis (in its chronic forms), 
pain is comparatively slight except on use, and other features will 
be of more use in diagnosis. The exact situation of the pain is a 
matter of great importance, for an abscess in a bone near a joint 
(especially true of the knee) has frequently been mistaken for joint 
trouble. If care be taken to examine for local tenderness, especi- 
ally on tapping the bone a little way off the joint, the error will be 
likely to be avoided. 

Stiffness. — May be of any degree, from the absolute rigidity of 
bony anchylosis to a little difficulty in commencing movement. In 
its milder forms, associated with some pain and aching, it may be 
merely the stiffness of some unwonted exercise. When this is the 
case it will usually be found that it is really the muscles and not 
the joint (though the latter has been accused by the patient) that is 
the seat of the pain. In any case, there will be the history of the 
exercise to guide us, and in a few hours, or days at the outside, it 
will subside. On the other hand, it may persist or get worse, and 
then we are faced with two alternatives : ( i ) it may be that the 
exercise (if there be a history of such) has excited a slight attack of 
synovitis : there will then be detectable a little effusion in the joint, 
or local heat, or grating near the joint (teno-synovitis), with con- 
siderable pain; (2) especially if there has been no unusual exercise 



vii AFFECTIONS OF JOINTS 231 

we must be on our guard, and look out for an oncoming attack of 
sub-acute or acute rheumatic fever. The thermometer will in this 
case show a slight (may be severe) pyrexia up to ioo° or 101 . If 
there is no rise of temperature, the nervous system must be carefully 
examined, especially for sensory changes and, round the joint, 
atrophy of structures, etc. Should we still get a negative reply to 
our investigations, we have probably to deal with a subject of the 
arthritic diathesis {vide p. 244). 

In its more chronic and definite forms the stiffness only appears 
after an attack of actual joint trouble, and then becomes chiefly of 
surgical interest, to ascertain what precise structures are involved, 
and how the stiffness can best be relieved. By this time, i.e. with 
a chronic stiffness, the history will probably have cleared up the 
etiology ; but if this be unobtainable or unreliable, we may bear in 
mind that (a) bony anchylosis is most likely to have arisen from 
severe traumatism, recovered tubercle, or pyaemia, doubtfully in- 
cluding gonorrhoea ; (b) bony obstruction without union, from 
rheumatoid arthritis, or from a Charcot's joint with excessive pro- 
duction of bone ; (c) thickening and stiffening of ligaments, etc., from 
gonorrhceal rheumatism, or chronic rheumatism, and possibly gout ; 
(d) stiffening of skin and other subcutaneous structures, from trau- 
matism (burns, etc.), in all of which characteristic features are nearly 
sure to be present (vide below under the appropriate heading). To 
determine whether bony union as opposed to bony obstruction is 
present complete general anaesthesia is often essential. 

Grating. — May be due to loose bodies in the joint and to acute 
synovitis, but in these two affections it can be produced by such 
manipulation of the joint as does not involve movement of the 
articulation. In the former case the history of the attack from 
which relief is sought is very characteristic. Possibly grating may 
have been previously perceived, but then has followed sudden fixa- 
tion with intense pain. In both of them the sensation conveyed to 
the hand is very different — less harsh, more like a tremor — to that 
which is felt when the cartilage is eroded, and two bony or rough 
uratic surfaces are rubbed on one another. This latter form of 
grating is only felt in gout, rheumatoid arthritis, or Charcot's osteo- 
arthropathy, and then the remaining factors are of more importance 
(vide below). 

Swelling. — The primary object in examining a swelling in or 
near a joint is to determine whether it is hard (bone, cartilage, or 
uratic deposit) or whether it is soft, probably fluctuating (synovitis, 
tubercle, sarcoma, aneurysm, etc.). Very slight examination will 



2 32 DIFFERENTIAL DIAGNOSIS chap. 

soon determine this point. If the swelling be hard (due to bone 
cartilage or intraosseous sarcoma) it may be due to (i) Charcot's 
joint, in which case the lumps will be loose and movable on one 
another, and the joint will be usually more movable than natural ; 
(2) osteoarthritis, when it will be more a lipping of the cartilage, 
an exaggeration of the natural outline of the articulatory ends of 
the bone, and the joint will have a less extensive range of movement 
than usual; (3) intraosseous sarcoma — this will be detected by 
the swelling being a little below or above the joint — of the bulk of 
the bone as opposed to its free edges — and possibly may give egg- 
shell crackling. A uratic deposit will also be hard, but its white 
appearance (or even discharge from a small opening) will scarcely 
allow of a mistake being made. 

If the swelling be soft (or fluctuating) our first object is to 
determine whether it arises outside or inside the joint, or both. If 
purely outside a little care will usually reveal the outlines of the 
articulation, or a little pitting on pressure (the hip and shoulder 
offer almost insuperable difficulties in deciding this point), the arti- 
culation itself will usually work smoothly (in the hip and shoulder 
this will be the best test). If purely from within, or from both, the 
outlines of the articulation will be obscured more or less in some 
positions of the joint ; this point is, however, more difficult in theory 
than in practice. In swelling outside the joint we may have to deal 
with aneurysm or sarcoma of the bone or bursal enlargements ; the 
former, unless cured or ruptured, will not only be soft, but have an 
expansile pulsation of its own ; sarcoma will have enlarged the bone 
some little way from the joint, while the contour of the joint itself 
may still be made out. Such are the principal points in typical 
cases, but in some unusual ones the diagnosis will require many 
examinations, and even then still be left in doubt ; for Bursal En- 
largements, vide below. 

In a swelling which involves the interior and exterior of a joint, 
traumatism, gout, and gonorrhceal rheumatism come in chiefly for 
consideration. Traumatism will be determined at once by the 
history ; for Gout and Gonorrhceal Rheumatism, vide below. When 
we have determined that we have to deal with soft material entirely 
inside a joint, pus, clear synovial effusion, and granulation tissue 
require to be differentiated. So far as the effusion itself is con- 
cerned we cannot decide between pus and clear fluid, but other 
points will leave little room for doubt between pyaemia and simple 
synovitis. Between an effusion and a growth of granulation tissue 
differentiation is usually tolerably easy, either by the pulpy semi- 



vii AFFECTIONS OF JOINTS 233 

fluctuating feel of the swelling, or (in the knee) by ascertaining 
whether the patella can be " rung " on the femur, i.e. whether we 
can feel bone knocking on bone, or whether some soft material 
comes in the way, as though the patella were depressed on to a soft 
cushion as it were. 

Bursal Enlargements. — Are either (1) quite isolated, i.e. not 
communicating with the joint, or (2) provided with an opening into 
the synovial cavity. In the former case difficulties of primary 
diagnosis can hardly arise, for the swelling will be readily movable 
on the tissues which surround it and the joint ; it will be incapable 
of compression, though probably fluctuating, while the outlines of 
the joint itself will be readily distinguishable, and its movements 
smooth. Communication with the joint cavity will be ascertained 
by examining the swelling in many positions of the articulation, 
when it will be found that in the position of greatest capacity — 
usually one of semi-flexion — the cystic swelling becomes more lax, 
its contents can be, partially at least, transferred to the joint and 
again expelled by a wide alteration in the position of the joint. 

Heat — Distinctly appreciable by the hand as a contrast to the 
general heat of the skin, will only tell us that the condition is 
acute ; in chronic joint troubles local heat is practically absent. Of 
acute affections, the heat is remarkable in gout and sometimes in 
pyaemia ; in traumatism it is fairly well marked as a rule, but in 
rheumatism is either practically absent (milder or more chronic 
cases) or is very little noticeable owing to the great general heat of 
the skin. 

Redness. — Is a pretty sure indication that the trouble is not 
purely intra-articular. Thus, it is scarcely, if at all, present in pure 
rheumatism (a synovitis) in simple synovitis, either acute or chronic; 
in gonorrhceal rheumatism (a pan- and periarthritis) it is commonly 
fairly well marked, but in gout it assumes its most intense and 
remarkable degree with a peculiar shiny condition of skin hardly 
seen in any other form of arthritis ; in fact, if a bright red, shiny 
condition of the skin over and round a joint has appeared within a 
few hours, with intense agony, in a patient previously in fair health, 
it is almost pathognomonic of gout ; the only alternatives are 
traumatism, of which the history will be obvious (and even here we 
must remember the frequency with which slight traumatism will 
excite acute arthritic gout), or less commonly pyaemia, and here 
there is not likely to be a freedom from previous symptoms of 
pyasmia, a definite source of the infection will usually too be fairly 
obvious, e.g. a wound, parturition, etc. 



234 DIFFERENTIAL DIAGNOSIS chap. 

Individually, then, it will be seen that these local physical signs 
are rather frail reeds to rely upon for a diagnosis, but collectively 
{vide below) they form a strong foundation, and especially when 
considered in the light that the history of the case can throw 
upon them. In this history the following points are the most 
important : — 

i. In the Family History. — Gout, rheumatic gout (probably 
rheumatoid arthritis), or rheumatism and its allies — chorea, morbus 
cordis, etc. — in very near relatives {vide below, Arthritic Diathesis). 

2. In the Previous Personal History. — Excess of eating or 
drinking (especially beer) make gout seem more probable; chorea and 
definite cardiac disease make rheumatism likely ; previous attacks 
of joint trouble similar or dissimilar to the present one will also 
have great weight. 

3. In the History of Onset — 

(a) Traumatism to the joint is obvious enough, but 
traumatism to a nerve (and other definite nerve 
diseases) must be noted as a possible causative 
factor. 

(i>) Exposure, either general or local (of a limb), is likely to 
produce a fairly sudden onset of rheumatism or acute 
synovitis. 

(c) An attack commencing during sleep is ipso facto likely 

to be gout. 

(d) Whether more than one joint was simultaneously or in 

rapid (i.e. a few days) succession attacked. Gout, 
gonorrheal rheumatism, acute synovitis non-rheuma- 
tic, tubercle and Charcot are commonly, at any rate 
in first attacks, monarthritic. Rheumatism or rheu- 
matoid arthritis is nearly sure to be at the bottom of 
a primary polyarthritis. 

(e) Which joint or joints are affected. The proximal 

phalanx of the big toe is especially obnoxious to first 
attacks of gout, the knee to gonorrhceal rheumatism, 
the middle or proximal phalanges of the hand to 
rheumatoid arthritis, though of course exceptions are 
numerous, and the more so the greater the number of 
previous attacks. 
(/) In cases where the patient is seen in a second (or higher 
multiple) attack, an equally careful account of the first 
one must be recorded if it can be possibly attained. 



vii AFFECTIONS OF JOINTS 235 

We may now consider the obverse side of the case, and briefly 
enumerate the main diagnostic points of each individual trouble, 
commencing with the most easily differentiated. 

Charcots Osteoarthropathy of Tabes. — Rapid (a few months or even 
weeks) onset of a nearly painless (so far as the joint itself is con- 
cerned, but lightning pains in the limbs very common) effusion 
into a joint, and excessive mobility of the articulation, should make 
a brief examination of the nervous system at once obvious to the 
mind. I am not aware that the joint changes are ever the first and 
only signs of tabes ; loose bony outgrowths, and (or) atrophy and 
total disorganisation of the original articulatory surfaces are the 
principal anatomical changes. Some cases of rheumatoid arthritis 
so closely resemble in their local effects a Charcot's joint, that an 
idea is existent that the two diseases are alike in pathology ; even 
granting a local identity, the remaining physical signs of tabes if 
present must always, I think, compel a diagnosis of Charcot, especi- 
ally if only one (or two) joint be affected. 

Flat Foot. — Requires to be mentioned in this connection because 
the patients so frequently come to us complaining of " rheumatism " 
in the ankle, and often pain up the calf of the leg. The patient 
will probably be a young and over-worked adolescent, and the pain 
will only be felt on or after long standing on the feet. Examination 
of the foot will show that the ankle is free from all signs of disease 
(heat, swelling, etc.), and that the pain is really in the scaphoid or 
head of the astragalus ; the arch will be seen to be obviously fallen 
in — footprints (from a wet foot) may be taken to show this more 
accurately. A complete absence of pyrexia, or general constitutional 
symptoms, will practically, with the above, settle the diagnosis. 

Gonorrhoea! Rheumatism. — Is apparently in its essence a mild 
form of pysemic joint. In its early stages will always, by the 
patient, and frequently by the medical man, be called rheumatism ; 
in fact, I know of no pathognomonic sign in this stage to differentiate 
it, for the local processes are then identical. Later, it will be more 
likely to be thought of by (1) its obstinacy to remedies; (2) its 
confinement to one joint — usually the knee — without others being 
successively attacked during a rapid subsidence of the first ailing 
joint ; (3) the implication of the outer structures of the joint, so that 
definite redness, slight oedema, and an angry, suppurative appearance 
supervenes ; it is a curious fact that actual pus never does form 
in these cases. Once these phenomena have started suspicion, 
inquiry must be made as to a present or recent — the arthritis is 
commoner in the chronic stage of gleet — gonorrhoea or vaginal 



236 DIFFERENTIAL DIAGNOSIS chap. 

discharge. In the absence of more serious signs of pysemia, the 
above points will be sufficient to complete the diagnosis. We may 
tabulate the points of difference between simple and gonorrhceal 
rheumatism thus : — 

Simple. Gonorrhoeal. 

May or may not have a gonorrhoea Certainly has either an active 
or gleet ; the gonococcus is not gonorrhoea or more probably a 

protective against the rheumatic subsiding gleet, 

poison. 

Pyrexia smarter and nearly sure to Pyrexia may be absent, if present 
be present. will be more irregular but per- 

sistent. 

Polyarthritis, many joints recover- Probably a monarthritis, if a poly- 
ing and getting worse coincidently arthritis all the affected joints 

or consecutively. became implicated before any 

one of them got well. 

If sweating at all it is profuse, and If sweating at all it is that of 
will go on all day ; smells sour. pyaamia ; worse at night or on 

falling asleep. 

Simple synovial effusion inside the Inflammatoryaffection of all tissues 
joint. in and round the joint. 

Traumatism. — In an acute attack the history is of course obvi- 
ous ; but it must not be forgotten that slight (or severe) traumatism 
may be the starting-point of acute gout, or of any of the more 
chronic joint troubles ; and therefore when we are called upon to read 
the riddle of a chronic arthritic trouble we must not rest too satis- 
fied with "traumatism," but must search the more carefully for a 
possible nervous (chronic degeneration) or constitutional (heredity, 
dietetic, toxaemic, etc.), element which has thus prominently ex- 
hibited itself in a damaged organ. 

Hysterical Joint Complaints. — This is a comparatively rare form 
of neurosis, at least in a severe degree, found almost exclusively in 
the female sex, and in young adult life (say seventeen to thirty-seven), 
and more frequent in the knee than elsewhere. Its principal char- 
acteristic is that the patient complains most bitterly of the severe 
pain in the joint, but on examination there is not the slightest 
sign of anything being wrong with the structures (nor with the hip 
when the pain is in the knee) — no heat, no swelling, no grating ; it 
will then be found as an almost pathognomonic feature that the 
pain is just as severe on slight touch as when the joint is firmly 
handled, and that when the patient's attention is engrossed in some 



vii AFFECTIONS OF JOINTS 237 

other direction the pain on manipulation disappears. Frequently 
complete anaesthesia is required to eliminate some form of anchy- 
losis, so resolute is the patient in preventing a movement, the 
slightest sign of which she finds exquisitely painful. If under an 
anaesthetic there is any effusion or grating, in fact anything patho- 
logical to touch, it is certainly not a case of pure neurosis. 

Synovitis, Simple, Acute, and Chronic. — An acute synovitis with 
effusion, without any ostensible cause except local exposure, is 
described, though personally I have not seen a case. In its local 
manifestation, it is said to exactly resemble acute rheumatism, but 
without its general symptoms. A chronic synovitis is by no means 
so rare ; it is usually started by some slight injury, and is probably 
maintained by continued use of the joint. It is characterised by 
being confined to one joint, associated with no general symptoms ; 
it consists of a simple distension of the synovial cavity (possibly, 
especially in the knee, commencing with an external bursa) ; there 
is very little pain, except on excessive use of the joint. As it 
occurs in practice, the only difficulty in diagnosis arises when the 
distension has become so excessive as to loosen the articulatory 
ligaments, when it may be mistaken — especially as pain is so slight 
— for a Charcot's joint ; the absence of any confirmatory signs of 
tabes should prevent mistakes. 

Tubercle. — Offers many cases of doubt in the early stages, in 
fact, there is at first nothing pathognomonic about it. That this 
must be so is obvious if we bear in mind the morbid anatomy of 
the trouble. The arrival in a joint of a company of tubercle 
bacilli is not announced by anything more than microscopic 
changes of a very low degree of inflammatory character ; in this 
stage it is a matter of minute cell changes which sound the alarm 
by twinges of pain. It is only when the granulomata have, by 
a growth and aggregation, reached a macroscopical size and bulk, 
that changes to the examining (from without) eye or finger are to 
be found. It may commence apparently either in the bone or 
synovial membrane. When in the former, we suspect its presence 
by the pain and starting in the joint being very much worse at 
night, and from the fact that this pain has arisen — in one joint 
only — spontaneously, or from traumatism so slight that there is 
very great discrepancy between cause and effect. When in the 
synovial membrane, there is as yet nothing to distinguish it from 
simple synovitis. As time goes on, however, we get suspicious, 
because this apparently trivial joint mischief will not subside ; we look 
around, and find that the patient — probably from the first a frail- 



238 DIFFERENTIAL DIAGNOSIS chap. 

looking object — is getting paler and thinner, inclined to mope, and 
capricious in appetite ; we hear of consumption in near relatives ; we 
notice that the joint is semi-voluntarily held in a constant fixed 
position — that of greatest ease — the slightest disturbance from 
which causes pain. By this time we have a strong conviction that 
tubercle is at the bottom of the mischief, but it is only when pulpy 
masses can be felt in the joint (in the knee or elbow), or an abscess 
forms (in hip, ankle, etc.), or the tissues external to the joint 
become chronically affected (wrist, e.g.) that this conviction gives 
place to absolute certainty. 

Such is the common history of tubercular arthritis and of its 
diagnosis — let us hope that appropriate treatment will have begun 
with suspicion, not have waited for certainty. It must be remem- 
bered that now and again cases of fulminating tubercle, so to 
speak, are met with in which the joint very rapidly gets into a 
condition of acute panarthritis ; here it is only the absence of 
any other plausible cause, and the persistency of great thickening 
long after the subsidence of acute inflammatory symptoms that will 
help us. For details of individual joints text - books of surgery 
must be consulted. 

N.B. — There is one great caution to give in dealing with 
tubercular arthritis, and that is not to exclude tubercle because 
the patient is old ; the disease is very common in elderly people in 
proportion to numbers alive. 

Rheumatism. — Consists in its morbid anatomy of a simple synovitis, 
so far as the joints are concerned ; and without other factors are at 
work, I believe, never alone gives rise to any other change. Typical 
acute or sub-acute rheumatic fever, with its pyrexia and sour sweats 
in adults (often, too, with endocarditis), or with its endo- or (and) 
pericarditis, or pleurisy, or history of chorea in children, consisting 
of a simple effusion, with pain running from joint to joint, some 
convalescent or well, while others are being attacked, cannot be 
mistaken for anything else. Its aberrant and chronic forms can 
better be discussed with differential diagnosis below. 

Gout. — In the joints is essentially associated with, if not actually 
caused by, a deposit of urate of sodium in the articular cartilages. 
It, with its sudden onset during sleep, the intensity of the pain, the 
vivid red and shiny appearance of the joint, is equally difficult with 
rheumatic fever to confuse with any other trouble. For doubts 
and difficulties, vide below. 

Rheumatic Gout. — The very existence of such a disease is 
denied by many, who dub it the refuge of the diagnostically desti- 



vii AFFECTIONS OF JOINTS 239 

tute. For myself, I certainly feel inclined to admit its existence, at 
least the existence of more than one factor producing the joints 
called rheumatic-gouty; though I must admit that many such 
cases are nothing but gout, and many are true rheumatoid 
arthritis (vide below). 

Rheumatoid Arthritis ; Osteoarthritis, better Chondroarthritis. — 
This is essentially at its commencement a degenerative proliferation 
of the cartilage cells, with an increase in the bulk of the articular 
cartilages, " the ruling passion — of reproduction — strong in death," 
but the result is poor stuff, with early decay and death stamped on 
it at its birth. There are two fairly marked types, (1) with (2), 
without marked inflammatory reaction in the other structures of 
the joint, especially of the synovial membrane. The former is 
mainly found when the disease attacks young people (it is most 
important to remember that this affection is, aye frequently, seen 
in young people, even in children) ; the latter is the commoner type 
in elderly and old patients, though here, too, it may have been pre- 
ceded by attacks of the more inflammatory type. The principal 
characteristics of both forms — when the acute features have passed 
away in the one, and under ordinary circumstances in the other — 
are (1) the lipping of the cartilages, so that the outlines of the 
joint are felt in bolder relief than usual; (2) grating in the joint; 
(3) stiffness and diminished mobility ; (4) frequently, and especially 
in the metacarpo-phalangeal joints, a subluxation of the articulation, 
so that the distal bones are diverted from their natural direction. 



Differential Diagnosis of the Last Four Affections, viz. 
Rheumatism (Acute and Chronic), Gout, Rheumatic 
Gout, and Osteoarthritis 

We may consider this as it occurs in the several epochs of the 
affections : — 

1. On the post-mortem table. 

2. After treatment has been tried for a little while. 

3. During a first attack. 

4. In a period of quiescence after a first attack. 

5. In subsequent attacks. 

1. On the post-mortem table. — This method of diagnosis comes 
in very late for purposes of clinical medicine, and is only occasion- 
ally able to give us information which is of use in estimating the 



2 4 o DIFFERENTIAL DIAGNOSIS chap. 

morbid condition in the earlier affections of other patients. The 
reasons why it is of such comparative uselessness are : (i) that the 
troubles under consideration are practically never fatal (a few cases 
of rheumatic fever must be excepted) in their earlier stages, when 
commencements of morbid changes could be usefully studied ; (2) 
that when the advanced conditions are found, after death from 
other diseases, the history of the joint complaints has been 
unrecorded or lost from the overwhelming interest or importance of 
the later disease. However, the facts are very simple, and diagnosis 
thus made is easy enough : — 

If urate of sodium be present in streaks or patches on the 
cartilages, we know for a certainty that gout has been at work, 
either alone or with other factors. 

If the cartilaginous coverings of the bone inside the joint are 
worn away, and the bare bony surfaces are eburnated or polished, 
and there are no traces of urates about, we know for a certainty 
that osteoarthritis has been the disease. 

If both the above changes, viz. urates and eburnation can be 
seen, we are justified, I think, in assuming that the morbid physio- 
logy of both, i.e. gout and rheumatoid arthritis, diseases has existed, 
and the more shall we think that osteoarthritis has been present the 
larger the superficial area of the end of the bone, this being the 
final representation of the pathological growth of the cartilage at 
the edges of the articulation — the lipping to be felt during life. 

If the disease has been a pure rheumatism — even chronic — we 
shall find very little or no organic change. In the acute affection 
there will be but clear fluid in the joint, with very little (probably 
none) congestion of the synovial fringes. In the more chronic 
condition of rheumatism there may be a little stiffening of the 
ligamentous structures of the joint, difficult to appreciate, and it is, 
I think, here possible to meet with a slight loss of cartilage, sug- 
gestive of osteoarthritic changes, for I believe that the frequently 
repeated onslaughts of pure rheumatism may by their local influ- 
ence initiate (? carry to their final stages) those changes which in 
osteoarthritis are started and carried on by loss of trophic nerve 
control. 

[If the cartilages are gone, the bone bare but not eburnated, 
rather cancellated (rarefactive v. sclerosing osteitis), and loose bits 
of bone are found, and the joint flail-like, we infer that it is a 
Charcot's joint ; though in dried specimens without any history 
we must not forget the probable identity of cause (i.e. loss of tro- 
phic influence) between this and osteoarthritis, and therefore the 



vii AFFECTIONS OF JOINTS 241 

possible identity of result ; though I think a true Charcot never has 
eburnation.] 

2. Inferences from Treatment. — This method again may be 
looked down upon as coming a little late in the day ; but we may 
urge that as medicine is not, and can never be (pace the scientific 
pharmacologists and physiologists) an exact science, and as there- 
fore treatment often has to be started on empirical supposition, it 
is but fair to allow us to gather information as to diagnosis as we 
proceed ; and to use the influence of one form of treatment over a 
joint affection as a starting-point for endeavours to make a complete 
deduction as to the nature of such affection. Salicylate of sodium 
is the drug above all others which is now likely to be tried in all 
doubtful cases of joint trouble, and so great is the influence of this 
drug (amounting almost to a genuine specific) over pure rheumatism, 
that it has become a nearly fixed article of medical faith that " the 
greater the relief afforded to pain, pyrexia, and general discomfort, 
the greater the share of rheumatism in the production of the 
trouble." If the relief be speedy and complete, the diagnosis of 
pure rheumatism is assured ; if relief be not at least very marked, 
we at once suspect, no matter what the age of the patient (I have 
already noted the frequency of acute symptoms of rheumatoid 
arthritis in young subjects), that there are factors in the trouble 
which are likely to lead to permanent changes in the joint, and 
consequent crippling ; we must carefully search for a gonorrhoea or 
gleet, and inquire more anxiously into family history. There is one 
important exception to be made to this usual rule of the influence 
of salicylates over rheumatism, viz. that if rheumatism attacks an 
individual who has had a long or severe drain on his constitutional 
strength, we find salicylates much diminished in utility or even quite 
useless ; I have met with such cases in women after prolonged 
lactation, in adolescents who have been poorly fed for years, and I 
suspect that in the rheumatism so common after scarlet fever the 
same conditions may hold. 

3. During a First Attack. — This is naturally the time when 
diagnosis is most required ; more perhaps for the sake of our own 
reputations as prophets, and for the advice we are to give as to 
warding off future or progressive trouble, than for the immediate 
sake of the patient, for whom any sensible treatment is little likely 
to be at once disastrous. The previous paragraphs on symptoms 
and pathology have already indicated the directions in which diag- 
nostic aid is to be sought, but for the sake of emphasis we may here 
tabulate some of the cases, and offer a few general remarks. 

R 



242 



DIFFERENTIAL DIAGNOSIS 



In young subjects — say under twenty-five — gout is so rare that 
unless it be a very typical case — nocturnal onset, one joint, intensely 
painful, very shiny and red — or unless there be a very strong and 
direct family history of gout, this disease may be excluded, and the 
problem — except for tubercle {vide p. 237) — becomes simple rheu- 
matism v. rheumatoid arthritis. 

They are alike in — 

1. Many (and any) joints are simultaneously or in the same 

attack affected. 

2. There is often effusion ; it is in the rheumatoid arthritis of 

young subjects that effusion is commoner, and that with 
pyrexia and general symptoms. 

3. The trouble appears to be a synovitis. 

4. There is no grating in a first attack. 



They differ in — 

True Rheumatism. 

Cardiac bruits and serous inflam- 
mation very common ; more com- 
mon the younger the patient. 

A sequence of joints very com- 
monly affected, so that different 
stages are found in the same 
case. 

Shape of joint pretty natural, ex- 
cept for effusion into its cavity. 



Sweating very common, and of a 
peculiar sour smell ; this is less 
marked the younger the patient. 

Fibrous nodules occasionally seen 
in fibrous tissue about a joint. 



Rheumatoid Arthritis. 

Cardiac bruits have no known con- 
nection with the affection, and 
if present have had a previous 
origin. 

Sequence of joints not well marked ; 
usually many at the same time, 
especially if the small joints are 
attacked ; very often only one or 
two larger joints affected. 

Shape of joint a peculiar spindle, 
as though atrophy above and 
below, and the joint enlarged in 
the middle ; especially notice- 
able in phalangeal articulations. 
This probably means that there 
is a slow outgrowth of cartilage 
before the symptoms, possibly 
also a slight atrophy of struc- 
tures above and below the joint. 

Sweating not a marked feature, 
and if present has no sour smell. 

Fibrous nodules not seen. 



vii AFFECTIONS OF JOINTS 243 

True Rheumatism. Rheumatoid Arthritis. 

Pyrexia and heat of skin usually Slight pyrexia may be present 
marked. though not common ; skin in 

general is certainly not hot to 
the touch. 

In middle age, or rather from twenty-five up to say forty-five, 
true gout becomes more frequent as the cause of a first attack, and 
according to my experience rheumatoid arthritis is less frequent, at 
least until thirty-five be past, when it again has an increase. It 
is between twenty-five and forty-five that I believe chronic rheuma- 
tism — a form without much pyrexia or swelling, only a little pain 
and stiffness — is a very prevalent affection ; though I admit it is 
very difficult to draw a hard and fast line between this affection 
and rheumatoid arthritis (vide Diathesis below). In old age, say 
from fifty-five upwards, I believe that first attacks of gout again 
become rarer, and that, too, in proportion to age, while (tubercle 
and) atrophic changes of an osteoarthritic or crippling character 
become the prevailing affection. 

4. In a Period of Quiescence after a First Attack. — It is in 
this period that we have to look out for stiffness, grating, or de- 
formity as evidence of the local trouble, and general symptoms 
that can be attributed to the constitutional affection of which the 
arthritic attack may have been only an outward manifestation. 

True rheumatism will have left practically no objective evidence 
of its presence ; a little stiffness and slight pain that gets less and 
less are its only sequelae. It may be, however, that slight pyrexial 
outbreaks, with a little local joint trouble, remind the patient that 
his disease is scotched only, and not killed; and these are the 
cases which, in my opinion, have a tendency to eventuate in crip- 
pling osteoarthritis as age creeps on. These, too, are the cases 
which in young people are so affected by changes in the weather. 
I believe that when a young person admits himself a living baro- 
meter he is the subject of true chronic rheumatism, which in his 
later years is likely to become crippling. Pleurisy, pericarditis, 
endocarditis, occurring on very slight or no provocation, will also 
throw light on the rheumatic nature of a previously doubtful joint 
attack. 

If the attack has been acute rheumatoid arthritis, the stiffness 
is never likely to so completely disappear ; a grating and deformity, 
with possible subluxation of joint, will probably soon make their 
appearance. On true rheumatoid arthritis my experience is that 



244 DIFFERENTIAL DIAGNOSIS chap. 

in young subjects weather has no influence ; it is only when age 
creeps on that such appears to be the case, but then I believe it 
is more due to the effect on senile tissues in general than on the 
joints in particular, and hence an elderly living barometer does not 
thereby tell us much to aid differential diagnosis. Beyond the 
obstinacy to treatment, and the local changes, there are no con- 
stitutional sequelae and complications. 

If the attack has been modified (typical will have been easily 
recognised) gout, then, as in epileptics, the patient will probably 
express himself as feeling very much better in general health than 
before the attack. Tophi must be carefully searched for, and the 
urine should be examined pretty frequently for any excess of uric 
acid or diminution in total nitrogenous output, hinted at by a low 
specific gravity. 

5. In Subsequent Attacks. — But little remains to be said under 
this head. If the history of the first attack (q.v.) be not available, 
the evidence from all sides — family, constitutional, and local — will 
have been steadily accumulating, and, though some features may 
still remain obscure, the main points — the tophi and urine of gout, 
the cartilaginous outgrowth of osteoarthritis, the morbus cordis 
with but slight local arthritic damage of rheumatism — will be almost 
sure to point only too clearly to the correct diagnosis. 



THE ARTHRITIC DIATHESIS 

Personally, I am indebted to the writings of Mr. J. Hutchinson 
for this expression ; that he was the first to utter it, is not likely, 
for the idea conveyed by it must have been present, one might say, 
for centuries, in the mind of the profession. Whatever its origin, I 
accept it as clearing up and harmonising many of the doubts and 
difficulties in arthritic diagnosis. 

I will first define precisely what I mean by the expression. It is 
this : that there are certain people who, owing to the intrinsic 
quality either of the joint structures (bones, ligaments, cartilages, 
and synovial membranes) themselves, or of the nerves which un- 
doubtedly govern their nutrition, find themselves in this position, 
— when from exposure, diet, or other unfavourable environment, 
a blood dyscrasia or other constitutionally morbid state arises of 
such a nature that some tissues are likely to suffer from imperfect 
nutrition ; the joint tissues above mentioned, or their nerves, are the 
parts of the organism upon which the stress will first fall : they are 



vii AFFECTIONS OF JOINTS 245 

the structures to suffer. Furthermore, when once such a morbid 
local process has been thus started in the joints, there is in these 
people (1) a greater tendency than in others for the process to 
extend ; (2) a probability that it will in this extension lose any 
possible specific character it may have originally possessed — gouty, 
rheumatic, etc. — and become generally and indiscriminately de- 
generative and destructive ; (3) a greatly diminished and less ready 
capability of repair if, and when, the constitutional dyscrasia has 
disappeared. Finally, to complete the story, I believe that though 
in the main such joint vulnerability is an inborn or hereditary — it 
may be from fairly remote ancestry — property of the individual, it 
may be acquired by personal habits and total environment (vide 
p. 7), and then in some degree (? crescendo) transmitted, but this 
transmission need not be an accurate and identical one, just as an 
epileptic need not necessarily have an epileptic child, but one that 
is generally weak in the nervous system ; so I believe a gouty or 
rheumatic ancestor may have generally arthritic descendants. 

These generalised laws or propositions which have been framed 
not by deduction — from few — but by induction — from many cases 
— constitute the explanation of the expression " crippling changes " 
which I have several times used, intending thereby to represent 
the generalised destructive processes which proceed from originally 
specialised causes. They explain the identity of the pathological 
anatomy of a Charcot's joint with that of an advanced osteoarthritic 
one, and of the latter with that of a chronic rheumatic joint in which 
the diseased process has overstepped its natural boundary of the syn- 
ovial membrane, and led to destruction of ligaments, etc. ; and this 
ultimate anatomical identity proves how impossible it is in chronic 
joint troubles to be certain that simple synovial rheumatism will 
not, clinically^ in the long run assume the features of rheumatoid 
arthritis. 

They possibly give us a clue to the reason why gonorrhceal 
rheumatism is so rare compared with a urethral discharge, and why 
tubercular joints are much less frequent than phthisis. 

Their bearing on the family history of a case of joint affection 
is important, but not decisive; they explain at once the "why," 
but they do not directly give us the " how," of a particular attack. 
There can be no doubt about the influence on diagnosis of a definite 
history of rheumatic fever, or of gout, in immediate ancestors or 
very close collaterals ; but when we hear that a father, mother, 
uncle, aunt, or grandparent had suffered at an advanced age from 
rheumatic gout, the specific indication is very much weakened, and 



246 DIFFERENTIAL DIAGNOSIS chap.vii 

we are thrown more completely on to local signs for the precise 
diagnosis ; a creaking, stiffened joint, a small tophus in the ear or 
elsewhere, a cardiac bruit, etc. In conclusion, let me emphasise a 
final statement — because or when we can find a hint of this pre- 
disposition we must not rest content with it, we must be all the 
more anxious to find the precise local factor in its earliest stages ; 
for it is only in these that treatment is even likely to be curative. 
When destruction is widespread and irreparable, precise diagnosis 
may be interesting scientifically, but it is of precious little use to 
our patients, who must ever be the first care in our minds. 



CHAPTER VIII 

DISEASES OF THE NERVOUS SYSTEM 

Section I. — Anatomy and Physiology of the Nervous System 

Before the problems of regional and pathological diagnosis of 
nervous affections can be intelligently discussed or tabulated, it is 
absolutely essential to sketch in slight detail the anatomy and con- 
nections of nerve structures, and the functions they are assumed or 
proved to possess. 

Recent researches into the microscopic anatomy of the nervous 
system have rendered it very probable, if not actually proved, that 
all nerve structures, without exception, from end bulbs or taste cor- 
puscles to cerebral hemispheres, are built up of neurons, and that 
these neurons or nerve units are all formed on the same structural 
plan, varying only in details of size of cells, length and number of 
processes, etc., and of course in physiological function. Each 
neuron, then, consists of: — 

(i) A Cell with Large Nucleus. — The substance of the cell 
shows a very fine fibrillar constitution with minute granules between 
the fibrillae. The body of this cell gives off — 

(2) Numerous Processes, all of which ultimately end in dendrites, 
and one at least of them becomes the axis cylinder of a nerve of 
ordinary anatomy ; this latter is spoken of as the neuraxon. 

(3) Dendrites. — An expression used to designate the extremely 
fine fibrillulae which form the final endings of all the processes of 
the neuron cell. It is by the interlacing of these dendrites — aptly 
termed by Foster a synapsis — that separate neurons are brought 
into physiological or functional connection with one another, though 
it must be clearly understood that no structural or anatomical con- 
tinuity has been proved to exist between the dendrites of different 
neurons ; in fact, the assumption is that dendrite acts on dendrite 



248 DIFFERENTIAL DIAGNOSIS chap. 

in a manner analogous to that of the action of the primary and 
secondary coils in an induction electric machine. 

The terminals of sensory organs and the end plates of motor 
nerves in muscles are probably nothing more than neurons of very 
abbreviated dimensions. With these exceptions, and possibly some 
in the cord and brain, all neurons possess processes of measureable 
length, and the neuraxons may be (as in the nerves of the extremities) 
many inches long ; but, except for this variation in length of the cell 
processes, they are all identical in structure, and collectively build 
up the whole nervous system. Accepting this as the anatomical unit, 
we may now proceed to consider how these units are combined. 



TABULAR VIEW OF THE ANATOMY OF THE 
NERVOUS SYSTEM 

A. End Orga?is or Terminals, each probably a very abbreviated 

neuron : — 

„ , (Voluntary muscles under control 

Contraction , ../ 

J of will 



In muscles in- 
tervening in 



„ . 1 Involuntary muscle fibres of heart, 

Relaxation. , , , ' . 

y blood-vessels, viscera, etc. 

■{ Sensation of nature and amount of contraction and 
relaxation of voluntary muscles = muscle sense. If 
such sensory structures exist in involuntary muscle 
they produce in health no percept on the general 
sensorium. 

{Touch. 
Variations in temperature. 
P * 
All other cutical stimuli. 
("Sight. 

3. In special sense organs sub- 1 Hearing. 

serving . . . . | Taste. 

(SmelL 

4. In glands and membranes /Absorption. 

governing .... I Excretion. 

5. In all other tissues of the body „ ' . , 
J ,. , , _. -l Growth, and 

superintending and regulating j n ' 

B. The Peripheral Nerves. — These are the main trunks (neu- 
raxons and collaterals) of the neurons • they possess dendritic 



DISEASES OF THE NERVOUS SYSTEM 



249 



endings, and synapses with the end organs ; they conduct stimuli or 
impressions to and from the end organs, thus constituting telegraph 
wires between the brain and cord and every part of the body. The 
exact anatomical relationship and distribution of the peripheral 
nerves constitute a branch of ordinary descriptive anatomy, an 
accurate and reliable knowledge of which is essential for the finer 
minutiae of the differential diagnosis of peripheral (and other) lesions. 
A detailed description would in this book be out of place. 

C. The Spinal Cord. — This constitutes a collection and primary 
arrangement of the connections between the brain and the periphery. 
A transverse section (or longitudinal one) accordingly presents a 
picture composed, so far as nervous elements are concerned, of 
certain groups of cells and bundles of fibres all cut in various sections 
according to their direction. Those groups and bundles, which are 
tolerably well known and understood, may be thus tabulated : — 



Cells of the Cord 



In anterior cornua (the main 
bulk of them, at any rate). 

In Clark's column. 



Others scattered through the 
gray matter, and possibly 
some of anterior cornua. 



O A 



Anterior roots or peripheral 
motor nerves, possibly also 
of vasomotor nerves. 

Nerves to and from viscera, 
and to and from direct 
cerebellar tract. 

Neurons or nerve-tracts, with 
origin and dendritic termi- 
nals totally within the cord. 



Fibres of Cord 



imn."| 

" J 



Posterior median column. 
Posterior external 
Posterior roots. 
Lateral pyramidal tracts. 
Direct „ „ 

Ascending antero-lateral tract 
of Gowers. 



Anterior roots. 
Direct cerebellar tract. 



Many unnamed fibres, both in 
white and gray matter. 



M 



<L> <U 



V O 



The ganglion on the posterior 
root of peripheral nerves. 

Rolandic or motor area of 

cerebral cortex. 
The reticular formation of 

medulla and pons, and also 

in the ordinary gray matter 

of cord, as intracordal 

neurons. 
Anterior cornua. 
Clark's column, and probably 

also cerebral and cerebellar 

cortex. 
In gray matter = intracordal 

neurons. 



'5° 



DIFFERENTIAL DIAGNOSIS 



D. The Medulla Oblongata. — Structurally, this is the continua- 
tion upwards of the cord, but the arrangement of its neuron cells 
and stems is more complicated and intricate. Only the more 
important (as far as our present knowledge is concerned) and 
apparently simple ones are here tabulated : — 

Cells of the Medulla 



Groups just below the floor of 
the fourth ventricle in serial 
continuation of those of the 
anterior cornua. 



f Funiculus gracilis. 
Groups m\ „ cuneatus. 
,, rolandi. 



Groups scattered through the 
reticular formation. 



■5 a 



Twelfth nerve, or hypoglossal. 

Eleventh nerve, or spinal 
accessory. 

Tenth nerve, or pneumogastric 

Ninth nerve, or glosso- 
pharyngeal. 

Eighth nerve, or auditory. 

Tracts to cortex of cerebellum 
and cerebrum, to the former 
bytherestiform body, to the 
latter through the reticular 
formation and fillet. 

Antero - lateral ascending 
tract. Posterior columns. 



Fibres of the Medulla 



Pyramidal tracts. 



o Motor cortex of brain. 



Funiculus gracilis. 


3 U 


,, cuneatus. 


_ V 


„ rolandi. 






B » 




<a C 




■£ '5 


Direct cerebellar tract. 


<D ^ 



Cranial nerves from sixth to 
twelfth. 



Posterior root ganglion, and 
also (above the cells of the 
funiculi) cells of cortex of 
cerebrum, and cerebellum. 

Clark's column, and also cere- 
bellar cortex. 



£ Cells in floor of fourth ven- 
S tricle. 



E. The Pons. — The main bulk of the superficially visible fibres 
run in a transverse direction ; the deeper parts are really the con- 
tinuation upwards of the medulla. The cells and fibres most essen- 
tially pontine are the following : — 



DISEASES OF THE NERVOUS SYSTEM 



251 



Cells of Pons 



Groups round the central 
canal. 

Groups in the roof. 



ftj3 «« ° 

£ « s .s 

W O) g >, 



Fourth nerve. 

Third „ (chief oculo-motor). 

Going to cerebrum and cere- 
bellum. 



Fibres of Pons 



Transverse. 



Cerebellum. 



Oblique. 

Vertical or pyramidal. 

Transverse and oblique, 
passing in all direc- 



ts tl 

■a b 



Cerebrum and cerebellum. 

Motor cortex of brain. 

Probably scattered through 
the whole cortex of cere- 
brum and cerebellum and 
formatio reticularis, and 
also basal ganglia. 



F. Cerebrum and Cerebellum. — In these organs the connections 
and arrangements of neurons attain their highest degree of com- 
plexity and obscurity. Some few we think we know, but of the 
vast majority our knowledge is practically nil. In the section on 
cerebral localisation more details of the anatomy and functions of 
the brain will have to be given. For our present purposes the fol- 
lowing table will be sufficient : — 

Cells of Cerebrum and Cerebellum 



Ascending frontal parietal 
and rest of motor cortex 
so called. 

Frontal lobes. 



I* 

3 -a 

ft 



Corona radiata, anterior two- 
thirds of posterior limb of 
internal capsule and pyra- 
midal tracts. 

Fibres running antero - pos- 
teriorly to opposite cerebellar 
lobes, and to the rest of cortex 
cerebri also. 



252 



DIFFERENTIAL DIAGNOSIS 



Fibres of Cerebrum and Cerebellum 



Of frontal, occipital, and temporo - sphe- Convolutions of same 

noidal convolutions. ^ side and of opposite 

o >« side (through corpus 

g j/> callosum). 

£ "u Convolutions of cere- 

° c bellum. 

of motor convolutions. ** ^ Gray matter of cortex. 

of internal capsule. g ■- 

, ,. , -v « rt / Frontal cortex, 

of anterior limb. I .5 « I ,. . 

... I rt <" ) Motor cortex, 

of posterior ,, anterior two-thirds. V 5; < „ . . , ,. 

_ r " . ,. , I « J Occipital andtemporo- 
of „ ,, posterior one-third. J i ., , * 

" " v J \ sphenoidal cortex. 

Note. — Between the anterior and posterior roots of the spinal 
cord on the one hand, and the cerebral hemispheres on the other, 
there is a total decussation of impulses, if not of actual fibres. But 
such functions and anatomical connections as the cerebellum exerts 
on, and possesses with, the cord are apparently not crossed. 

After this brief dogmatic sketch of the structural connections of 
the nervous system, we must proceed to a similar tabulation of the — 



FUNCTIONS OF NERVE MATTER 

We will commence as before with The Neuron. 

1. The Cell. — While there is still some dispute as to whether 
the cell possesses any function of a transforming or reinforcing 
character, there is unanimity in accepting a purely nutritive function 
as the chief, if not the only, function properly belonging to the cell. 
At any rate, it is a clinical fact that neuraxons, collaterals, and den- 
drites, and consequently the synapses of the dendrites, all undergo 
complete degeneration and death when separated from the neuron 
cell, or when the neuron cell itself is killed ; and nutritive disturb- 
ance of the cell is rapidly followed by similar changes in the other 
parts of a neuron, and structures (non-nervous, e.g. muscles) to 
which the nerves are distributed. 

2. Neuraxons and Collaterals. — The only ascertained function 
of these parts of a neuron is to transmit unchanged along their length 
impulses derived, or started (a) from sources external to the body, 
including in this term food in the alimentary canal, and air and its 
impurities in the air passages, as well as stimuli applied to the skin, 



DISEASES OF THE NERVOUS SYSTEM 



; 53 



etc., (b) from the synapses with dendrites of other neurons. They 
are thus purely and absolutely analogous to telegraph wires, carrying 
to and from every structure of the body messages which result in 
the performance of every possible physiological process, whether 
motion, perception, nutrition, secretion, etc. 

3. Dendrites, and Synapses of Dendrites. — It is by these we now 
assume that impulses are transmitted from neuron to neuron, and 
transformed in character. It would seem as though the synapses 
afforded an opportunity for a sort of inductive action of neuron on 
neuron; the actual resultant of any impulse from any source 
depending upon the inherent qualities of the neuron brought into 
induced action and its connections (a) with other neurons to which 
the impulse may be again transmitted, or (b) with terminal organs, 
muscle, gland cell, or other tissue capable of exhibiting a final 
resultant. 

Peripheral Nerves. — As these are simply neuron complexes, 
their functions in gross are those of their units ; in detail they 
carry the impulses which eventuate in — 

A. — Movements in Voluntary Muscles which — 



In Health. 

Are possible to an amount known 
by experience to each indi- 
vidual ; are under the control 
of the will, and capable of co- 
ordination for any purpose. 



In Disease. 

Are weakened, or absent, or inco- 
ordinated. 

J Time or order. 
\Amount. 
Involuntary (Tonic, 
spasms. \ Clonic. 



In volition 



B. — Sensory Perceptions — 

Excessive 
A known experience of the indi- Weakened 
vidual, differing materially in Lost 
different individuals. Delayed 

Perverted 



in /"Temperature, 
■relation-^ Pain, 

to [Touch, etc. 



C. — Reflex Processes, any of which may incidentally affect 
consciousness and become a percept. They are divisible into 
three groups : — 

Group I. — Experimental, or acting through cutaneous external 
stimuli : — 



254 DIFFERENTIAL DIAGNOSIS chap. 

Superficial — 

In Health. In Disease. 

Plantar, cremas- Present, but somewhat Obviously increased, 
teric, etc. variable in amount. „ decreased. 

Absent. 

Deep— 

Knee jerk. Present, but also some- Increased, diminished, 

Elbow jerk, etc. what variable. absent. 

Group II. — Natural from the viscera with contents or condi- 
tion for stimulus, and involuntary movement or secretion, etc., as 
the resultant. Of these there must be very many, but in only a 
few cases and conditions are of much use to us clinically : — 

In Health. In Disease. 

Those of bladder. Co-ordinated for pur- Inco-ordinated, and 

„ rectum. poses of voluntary often removed from 

micturition and de- voluntary control, 
faecation. 

Group III. — Vasomotor regulating the supply of blood to a 
part — 

In Health. In Disease. 

The essential point is the local control over This local control is fre- 
local blood supply. quently lost or per- 

verted. 

D. Trophic Influeyices. — Clinical evidence, as well as experi- 
mental, tends to suggest that, besides the above noted trophic 
influence of the neuron cell on its own processes, there are influ- 
ences constantly ascending and descending peripheral nerves which 
are essential for the proper nutrition, growth and decay of the 
structures which, in their ordinary functions, are under the control 
of the nerves distributed to them — muscles, for instance, or sensory 
end organs, glands, etc. — and there is a certain amount of evidence 
to show that these influences are something active, liable to excess 
or perversion, as well as absence, for it is found that irritation or 
inflammation of nerve structures is more effectual in producing 
destruction or degenerative effects than is mere section of a nerve 
trunk. Illustrations of trophic changes will be noted presently 
{vide p. 266). 

E. — Special Sense Nerve Phenomena and Mental Processes. — These 



viii DISEASES OF THE NERVOUS SYSTEM 255 

will be noted when the brain is under consideration. We may 
here merely mention — 

Hearing . J . And in disease may be increased, 

Taste f , T T * perverted, or diminished. 

Smell J health - 

Spinal Cord. — To enumerate in detail the functions of the 
cord would in large measure be to repeat what we have said on 
peripheral nerves. Its cells are constantly engaged in the task of 
superintending the nutrition of peripheral nerves and other struc- 
tures, as well as of intracordal fibres or neurons, as has already 
been noted. The principal function of the cord, as a whole, is to 
act as a sort of subordinate office to the brain's head office, and by 
its complexes of neurons to arrange and co-ordinate impulses 
passing through it. Thus it is the final manager of efferent 
impulses to voluntary muscles arranging their order ; it is the 
primary manager of afferent impressions, enabling our minds to 
become precisely and accurately conscious of our environment; 
and lastly, it possesses innumerable mechanisms for the perform- 
ance of reflex functions of all descriptions : and these may (a) be 
performed entirely by the cord without notification to the sensorium, 
or {b) cause such notification so that we perceive the reflex, but (c) 
they are always liable to control from the head office of the brain 
under all circumstances. 

Brain, or Encephalon. — As the seat of what is termed the 
mind, the encephalon remains the supreme governor and controller 
of every process going on in the body. It is the head office to 
which all information from every part must be sent, whether we 
are conscious of such information or not, and it retains to itself 
the power to intervene in and control everything, . but allows 
generally to the cord a very large measure of home rule in those 
processes which are mainly concerned in the mere sustentation of 
the animal framework. 

Having thus considered anatomical structure and physiological 
function as separate entities, we have now to associate the two into 
mechanisms for purposes. This, even in the peripheral nerves, is 
not always a matter of mathematical precision ; in the cord the 
difficulties become much greater, while in the brain they are as 
yet insurmountable except in a few special cases, and in a most 
general manner. We shall arrive at the most available certainty 
with greatest clearness by taking functions and tracing their path- 



256 DIFFERENTIAL DIAGNOSIS chap. 

ways ; the following tables are apparently reliable as far as our 
present knowledge goes, but being based upon clinical experience 
and experiment, are liable to some alteration as our knowledge 
grows in exactitude. 

Motor Tracts or Pathways of Voluntary Muscular 
Movements 

The nerve impulses are centrifugal ; so, taking the same course, 
we have — 

1. Highest volitional, or will centres of doubtful locality, prob- 

ably (according to Hughlings Jackson) the cortex of the 
frontal lobes. 

2. Rolandic region of cortex. 

3. Corona radiata. 

4. Anterior two-thirds of posterior limb of internal capsule. 

5. Pyramidal tracts — 

(a) In crura cerebri. 

(b) In pons. 

(c) In medulla (including the decussation). 

(d) In cord (crossed and direct). 

6. Cells of anterior cornua. 

7. Peripheral motor nerves. 

8. End plates. 

9. Muscles. 

In any given voluntary movement the parts played by these 
various structures are as follows : — 

In (1). — The wish starts by psychological processes or influ- 
ences from without, and takes a less amorphic shape as nerve im- 
pulses, which pass along the processes of the neurons concerned ; 
by dendritic synapses these impulses are transmitted or passed on 
to the neurons of the rolandic region. 

In (2). — These physical impulses are marshalled and co-ordinated 
in a manner that may be compared to the first sorting of letters at 
the General Post Office into those for each sub-district or " route," 
and just as by arrangement letters can be sent by an alternative 
route, when one is blocked, with slight resultant confusion in their 
delivery, so by the dendritic synapses of innumerable cortical 
neurons can these impulses be transmitted by other than the usual 
path, with resultant delay or disturbance in movement. Herein lies 



vni DISEASES OF THE NERVOUS SYSTEM 257 

the commencement of the explanation of the common statement 
that " Movements and not muscles are represented in the cerebral 
cortex (and cord)." Each neuron of the rolandic cortex has to 
share in many movements, but never completely causes one ; hence 
slight cortical damage is likely to impair many movements, but not 
absolutely to paralyse any. 

From (2) impulses pass through (3), (4), and (5) in a compara- 
tively simple manner along the neuraxons, and break on the 
complicated synapses of their terminals with the dendritic com- 
mencements of (6). 

In (6), with its connections, goes on the final sorting of impulses 
for delivery along the neuraxons of the appropriate members of 
(7); thus is completed the explanation of the statement inserted 
above relative to movements rather than muscles being represented 
in brain and cord. 

Along (7) messages are carried again in a very simple manner 
to reach (8) and (9), and produce in them appropriate reaction. 

For clinical diagnosis it is important to note the absolute inde- 
pendence of the nutrition and life of the neurons of (1), or level A, 
of (2) to (5), or level B, and of (6) to (9), or level C. A lesion of 
destructive character in level A leaves the mechanisms of levels B 
and C, qua a piece of machinery, quite untouched and ready to 
start and carry out co - ordinate movements, provided only that 
impulses can reach them somehow; and, similarly, B and C are nutri- 
tionally quite independent ; hence we find at the bedside that a 
paralysis due to lesion in level C is characterised by the flaccidity 
with rapid wasting of the affected muscles, and probably other 
trophic disturbances of the skin and its annexes. A paralysis due to 
a lesion in levels B or A is characterised by retention of the tone and 
of volume of the affected muscles, and absence of trophic disturb- 
ance of other structures. 

Sensory Tracts or Pathways of Afferent Impressions 
from without 

These impulses are centripetal, and hence we begin with — 

1. Peripheral sensitised end organs in skin, muscle, or special 

sense mechanisms (these are the best understood clini- 
cally and microscopically, but analogous nerve structures 
must exist in every tissue and gland of the body). 

2. Sensory nerves of descriptive anatomy. 

s 



258 DIFFERENTIAL DIAGNOSIS chap. 

3. Cells in the ganglia on the posterior roots. 

4. Posterior root of spinal nerve. 

5. Posterior columns of cord, external and internal, and 

probably also Gowers' antero-lateral tract, and the direct 
cerebellar tracts. 

6. Cells in funiculi gracilis, cuneatus, and rolandi, and also 

Clarke's column. 

7. Cells and fibres in formatio reticularis and fillet of medulla 

and pons, tegmentum of crus cerebri, inferior peduncle 
of cerebellum, and the cortex of both cerebrum and 
cerebellum. 

With regard to the part played by these various structures in 
the perception of an external stimulus, we are very much more in 
the dark than is the case with the corresponding motor tracts ; but 
the following statements would appear to be justified : — 

In (1) the external impulse, whether of touch, temperature, pain, 
etc., is received and converted into what we can only call a common 
nerve impulse, which is then carried by way of (2), (4), and (5), as 
along telegraph wires, until it breaks on the dendritic synapses of the 
terminals of these, and thus can impress itself in some way on the 
terminals of the neurons in (6) and (7). It is commonly assumed 
and universally accepted as a legitimate deduction from experiment 
and clinical evidence that Nos. 1, 2, 3, 4, and 5 form a lowest level 
or neuron complex, corresponding to the lowest level on the motor 
side, and that this lowest level is dependent for its nutrition on 
No. 3 ; the injury or destruction of which results in corresponding 
degeneration or destruction of the whole level. But after we leave 
this level precise knowledge ceases, and speculation reigns as to 
the number of serial neuron levels and as to the exact paths by 
which impulses reach the sensorium, and even as to the locality of 
the sensorium. And, again, as regards co-ordination of, or judgments 
upon external impressions, we only know that disease of the lowest 
level (as in tabes dorsalis) leads to great perversion of them ; e.g. 
a touch is referred to a totally wrong spot, but we do not know 
whether this lowest level is the only co-ordinator of afferent impres- 
sions, or even if it is the chief one. 

Reflex Paths 

So far as is known, there are no special paths reserved entirely 
for reflexes ; the impulses travel by the ordinary sensory and motor 



VIII 



DISEASES OF THE NERVOUS SYSTEM 



259 



nerves. We may, however, discuss a few points in this connection. 
For a reflex phenomenon we require a chain of structures which 
we may thus tabulate : — 



A sentient receptive 
surface or end 
organ on which 
the stimulus may 
act. 

An afferent nerve. 

A central connection 
of afferent and 
efferent mechan- 
isms. 



An efferent nerve. 



A terminal organ to 
exhibit the reflex, 
whatever its 
nature. 



Skin or external surface in the experimental 
class. 

Mucous membrane or epithelial cells in visceral 
class. 

Tissue elements (?) in vasomotor class. 

The ordinary afferent nerves of the organ or area 
in question. 

This, so far as we can judge, is not an organic or 
structural connection, but merely the functional 
synapses of the dendritic terminals of the re- 
spective sensory and motor neurons in the 
central system, allowing a transmission of 
impulse. 

The motor nerves of voluntary or involuntary 
muscles, corresponding to the class of reflex in 
question ; and nerves carrying efferent im- 
pulses for other organs. 

Voluntary muscles in Class I. 

Involuntary muscles, fibres, and epithelial cells 
of glands of viscera in Class II. 

Involuntary muscle fibre in arterial coats in Class 
III. 



For the reflex to take place it is essential that this chain should 
be complete in each link, and that there should be no strong in- 
hibitory influence at work capable of stopping the reflex. 

Class A. — The true or superficial reflexes may occur from any 
area of skin or from the conjunctiva. Those most commonly looked 
for are : — 

Plantar, involving health of 1, 2, and 3 sacral nerves and connections. 

Cremasteric „ „ 1, 2, and 3 lumbar „ „ 

Abdominal „ „ 8 to 12 dorsal and 1 lumbar „ „ 

Thoracic „ „ 1 to 8 dorsal „ „ 

Conjunctival „ „ 5 and 7 cranial „ „ 

but in special cases many others are looked for as indications of 
health or disease of specific nerves and segment of the cord. 

Of the so-called deep or tendon reflexes at knee, elbow, wrist, 
etc., we know that the path for them must, in some of its 
details, be different from that of the superficial ones, for the two 



260 



DIFFERENTIAL DIAGNOSIS 



can vary independently of one another in degree ; the knee jerk, 
for example, is often absent, while the superficial reflexes of the leg 
are still obtainable. The knee jerk has been more fully studied 
than any of them, and about it we may make the following state- 
ments, with deductions : — 



It requires for its production — 



the 



(i) A certain degree of myotatic irritability (Gowers) 

quadriceps extensor muscle. 
(2) The integrity of the third and fourth lumbar nerves, and 

their synapses in the cord. 

It is capable of being modified by influences from the en- 
cephalon, which influences are found to travel by the pyramidal tracts 
of fibres, and are believed to be of two kinds : (a) restraining from 
the cerebrum ; (b) reinforcing from the cerebellum (Jackson). 

As deductions from these premises — 

Diminished cerebral control. 

Increased cerebellar influence. 

Increased irritability in some link of the 

spinal and peripheral chain. 
Increased cerebral control. 
Diminished cerebellar influence. 
Diminished irritability (or break) in some link 

of the spinal and peripheral chain. 

When the knee jerk is found to be materially altered in character 
from an average expected normal, we should try and estimate 
which of these influences is at work. The common clinical examples 
are : — 



lcreased knee jerk 


(a) 


means 


(*) 




w 


iminished or ab- 


(a) 


sent knee jerk 


(*) 


means 


(c) 



Knee jerks increased 
from cause (a). 



Paralysing lesion of 
rolandic cortex, or 
internal capsule. 

Lateral sclerosis pri- 
mary. 



Old transverse myelitis 
above lumbar en- 
largement, causing, 
e.g., lateral sclerosis 
of lower part of 
cord. 



Indicated by 
Apoplectic seizure 
ordinary type. 



of 



Chronic history of in- 
creasing weakness 
and jerkiness in 
walking. 

History of acute para- 
plegia. 



DISEASES OF THE NERVOUS SYSTEM 



26: 



From cause (b). 



From cause (c). 

Knee jerk diminished 
or absent from 
cause (a). 



From (b). 



From (c). 



Occasionally apparent- 
ly in cerebellar tu- 
mour, causing more 
irritation than de- 
struction. 

Peripheral neuritis in 
early stages. 

Occasionally apparent- 
ly in tumour of cere- 
brum. 

Meningitis, vertical and 
even basic. 

In shock their absence 
is probably partly 
thus explained; gen- 
eral paralysis of in- 
sane in later stages. 

Occasionally apparent- 
ly in abscess and 
tumours that have 
destroyed some parts 
of cerebellum. 

Peripheral neuritis, later 
stages, acute or 
chronic anterior po- 
liomyelitis. 

Tabes dorsalis. 

Pseudo - hypertrophic 

paralysis. 
Myelitis of lumbar 

region. 



Indicated by 

Headache, vomiting, 

and optic neuritis. 



Pins and needles, and 

weakness. 
Headache, vomiting, 

optic neuritis, etc., 

Jacksonian epilepsy. 
Pyrexia with cerebral 

symptoms. 
Mental features. 



As above. 



Rapid or chronic wast- 
ing of muscles with 
R.D. 

Lightning pains; Argyll 
Robertson pupils, etc. 

Method of getting up 
from the floor. 

Acute paraplegia. 



In some of the above cases the meaning of the alteration is fairly 
clear and definite, but it must be confessed that in tumours and in 
inflammation within the cranium neither the result nor its cause is 
always very obvious. In epilepsy, again, the frequent absence, and 
in general paralysis of the insane the frequent exaggeration, are not at 
once readily explicable ; in hysteria the knee jerks are very variable, 
and I have, I believe, found them absent in an otherwise perfectly 
healthy individual. 

Class B. — Visceral. For the bladder and rectum (it would 
seem probable also that the rest of the alimentary tract and other 



262 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



viscera are under similar control by means of the appropriate sym- 
pathetic and ordinary nerves) it is assumed, with great probability, 




Diagram to represent nerve impulses concerned in normal micturition. 

that in the lumbar enlargement of the cord the synapses of the 
sensory and motor neurons of the lower sacral nerves (probably) are 
so arranged that afferent impulses, started by the condition or 



viii DISEASES OF THE NERVOUS SYSTEM 263 

contents of the viscus, on reaching the cord can, and do in health, 
diverge in three directions : one impulse or message goes by either 
the posterior or antero-lateral ascending columns of the cord to the 
sensorium, and there produces by appropriate synapses a wish to 
micturate or defaecate ; following this message to its termination, 
and supposing the nervous system is quite intact, the desire can 
result in restraint of the act or in the act itself, according as circum- 
stances of a social nature are unfavourable or the reverse ; the former 
being one illustration of inhibition {vide p. 267). In either case 
the messages (though of different import) pass down the pyramidal 
tracts (?) to the appropriate cells of the anterior cornua, and thence 
by peripheral neurons (1) to the voluntary abdominal muscles, (2) to 
the sphincter, and (3) to the detrusor musculature of the bladder, in- 
fluencing them in a manner appropriate to the control or permission 
of the act. The second and third divisions of the afferent message 
are, as it were, short circuited, passing simply into the cord by the 
posterior roots and immediately becoming transmitted by synapses 
to the efferent neurons controlling the sphincter and detrusor 
muscles of the bladder, and causing action or inaction of those 
muscles respectively. It is by this short circuit that micturition and 
defalcation are provided for in the absence of consciousness. A 
diagram shows this somewhat complicated description very simply. 

Theoretically, then, it is possible for the acts to be interfered with 
by lesions in any part of this course, but clinically such interferences 
may be reduced to one of four categories, which, with the possible 
explanation in each case, may be thus stated : — 

1. Retention of urine, distension of the bladder, with overflow 
and consequent constant dribbling. This is perhaps the commonest 
form, and is found under many widely different clinical circum- 
stances. Its possibility is due essentially to the fact that the 
sphincter fibres of the bladder are more powerful than the detrusor 
fibres. It occurs in — 

(a) Parturition, es- Probably then due to a spasm of the sphincter, 

pecially primi- produced locally by irritative prolonged pres- 

paras. sure of fcetus. 

(b) Operative pro- Probably due to intense reflex stimulus of unusual 

cedures about character through unusual channels, leading to 

perineum, etc. spasm of sphincter. 

(c) Tabes dorsalis Probably due to an inability of afferent messages 

occasionally. to reach the efferent neurons with sufficient 

energy. 



264 



DIFFERENTIAL DIAGNOSIS 



(d) Senile and other Probably the original fault lay with highest will 

mental condi- centres in checking the voluntary act from 

tions, especially deliberate motive ; this was followed by blunting 

so-called hy- of sensorium, while the sphincter still retained 

sterical. its ascendency in physical power. 

(<?) Enlarged pro- Difficulties probably purely mechanical and not 

state and stric- nervous at all, except that habit blunts the 

ture, etc. sensory terminals in the bladder. 

2. Complete incontinence, bladder never full, urine constantly 
dribbling as fast as it reaches the bladder. Indicates essentially a 
paralysis of the sphincter fibres. This form is rarely found except 



Acute transverse Due to destruction of the motor efferent neurons, 

myelitis of lum- and consequent absolute sphincter paralysis, so 

bar enlarge - that gravity causes the escape of urine, 
ment. 

It is a curious, but very important fact, that such absolute in- 
continence is never found in purely functional peripheral troubles, 
and only as the rarest of curiosities even in organic definite 
peripheral neuritis. 

3. A co-ordinated more or less normally complete emptying of 
the bladder without the intervention of the will or of consciousness. 
The occurrence of this form essentially indicates that the lumbar 
(sphincter and detrusor) centres are intact with all their reflex 
mechanisms, and proves to a demonstration that the higher centres 
are not essential for the act, but that the lumbar cord is quite 
competent when necessary to control the entire proceeding. It 
occurs pretty frequently, e.g. in : — 



(a) Nocturnal incon- 
tinence in chil- 
dren (enuresis). 

(/;) Transverse mye- 
litis above the 
lumbar enlarge- 
ment. 

(<:) Tumours and 
other forms of 
pressure, caus- 
ing paraplegia. 



May indicate unusually powerful stimuli (stone, 
hyperacidity, etc.), or undue irritability of the 
local nervous mechanism. 

Here it is a localising indication of the position 
of the lesion, and is of considerable value as 
indicating that the mischief has not reached 
the lumbar cord. 

Again a localising symptom of some importance. 



4. Slighter degrees of interference with co-ordinate micturition. 



DISEASES OF THE NERVOUS SYSTEM 



265 



These form rather a heterogeneous group of cases in their outward 
manifestations. It includes : — 



Probably due to irregularity in arrangement and 
arrival of reflex messages on the afferent side. 



Probably the messages on the afferent side are 
abnormal in their meaning ; possibly also there 
may be local irritation of sphincter, so that 
distension with overflow may result. 

Indicates merely a little weakness of sphincter. 



Probably only indicate the great intensity of 
natural stimuli, the nervous mechanism being 
intact. 



(a) Tabes dorsalis 

with what is 
termed stam- 
mering blad- 
der ; may be 
present in other 
forms of sclero- 
sis of cord. 

(b) Temporary re- 

tention in spas- 
modic stricture, 
stone, etc. 

(c) Discharge of ur- 

ine on cough- 
ing, especially 
in women. 

(d) Strangury and 

frequent mictu- 
rition of cystitis 
or of enlarged 
prostate at 
night. 

Although we have thus dealt at length with the bladder only, 
it is extremely probable that defecation is under precisely similar 
control, and worked by precisely similar mechanism ; but the 
clinical manifestations of its pathological performance are not so 
marked, nor so easily followed in detail. This is no doubt due in 
part to the greater capacity and distensibility of the colon, which 
acts towards the sphincter ani, like the body of the bladder to its 
sphincter ; but chiefly to the fact that the bladder is being constantly 
filled with a fluid secretion, while the rectum is being intermittently 
filled with a (more or less) solid material; a few doses of saline aperient 
will render the likenesses in action more apparent. 

Class C. — Vasomotor reflexes. Of the nerves and paths by 
which these pass we are profoundly ignorant, except that they seem 
to run in the so-called sympathetic chain, and to pass to and from 
the cord with the anterior roots. We recognise the loss of vaso- 
motor control in paralysed limbs and under many other conditions, 
but we are not able to make much clinical use of our observations 
as regards localising indications. 



266 DIFFERENTIAL DIAGNOSIS chap. 

From the fact that all reflexes may in health or disease be 
attended with sensory perception of their occurrence, it follows 
as a legitimate, and indeed inevitable deduction, that the path of the 
afferent impulse must have at least two dendritic connections in the 
spinal cord or central system : one with the appropriate motor 
neuron, and the other with those neurons which ultimately conduct 
an impression to the sensorium. An anatomical basis has been 
discovered for this deduction in the division of all afferent nerves 
into two branches — one going towards motor neurons, and one 
continuing in the direction of the sensorium. 



Seat and Paths of Trophic Influences 

But little can be said on this head beyond what has already 
been noted in the general description of a neuron and the functions 
of its component parts. It would appear that for the perfect nutri- 
tion of all structures they must have a perfect connection with a (at 
least one, and probably several) neuron cell, the physiological health 
of which they equally enjoy ; failing with it, and recuperating too 
with it. Obviously the most simple and uncomplicated evidence of 
this probable connection is most likely to be found and established 
in the case of the peripheral neurons of the limbs, the dendritic 
synapses and relationships of which are fairly well understood ; and 
the following clinical examples go far to establishing the general 
proof of the theory : — 

i. The rapid atrophy of the corresponding motor nerves and 
muscles (or parts of muscles) after complete destruction of all (or 
some) of the cells of the anterior cornua. 

2. The defective growth of all parts of a limb that has been in 
childhood severely paralysed by anterior poliomyelitis. 

3. The changes in the skin and annexa when the sensory nerves 
or cells on the posterior roots are damaged. 

4. The mysteriously rapid onset of bed sores from very 
slight causes (pressure, warmth, etc.) in many cases of acute 
myelitis. 

5. The equally malignant cystitis and renal trouble that so 
frequently accelerates or causes death in similar cases of myelitis, 
notwithstanding most rigorous asepticism in artificial emptying of 
the bladder. 

6. Certain very suggestive dystrophies after experimental divi- 
sion of nerves, e.g. the fifth cranial, etc. 



DISEASES OF THE NERVOUS SYSTEM 267 



Special Sense Tracts 

The olfactory, optic, auditory, and glossopharyngeal nerves 
require only to be mentioned here. Their connections will be better 
studied when dealing with the principles of brain localisation {vide 
Cranial Nerves, p. 303). 

These facts of anatomy and associated function form the main 
foundation upon which are laid the principles of differential 
diagnosis of nervous diseases ; but before proceeding to construct 
tables from them, there are a few general points and terms to which 
attention must first be directed. 

Inhibition and Interference 

By these terms are understood the power which one neuron or 
group of neurons possesses of so influencing another neuron or 
group as to check or interfere with in any direction the function 
which the second mechanism intrinsically possesses. This power 
may be exercised either voluntarily through the will, of which our 
daily actions are almost one continuous example, or it may be, and 
probably is, the inherent function of large numbers of neuron com- 
plexes which may thus act without any effect on consciousness, the 
most constantly occurring clinical example of which is the hy- 
pothecated influence of the cerebral and cerebellar cortex on spinal 
reflexes ; the former being supposed to check them, the latter to 
increase them. 

Inhibition and interference constitute almost insuperable diffi- 
culties in the way of drawing satisfactory and conclusive deductions 
from the experimental destruction of limited areas of nerve tissue in 
cord or brain. 

Direct and Indirect Symptoms 

By direct symptoms are understood those negative or positive 
morbid phenomena, directly appreciable by the observer, which 
arise as the direct result of destruction or irritation of a certain 
group of fibres with known definite function, e.g. blindness from 
laceration of optic nerve, noises from irritation of the auditory 
nerve, paralysis from the destruction of the pyramidal tracts, etc. 

Indirect symptoms, as the term is used clinically, are really of 
two kinds : (a) those which must be assumed to exist as the plainest 
corollary from the hypothesis of inhibition and interference, and 



268 DIFFERENTIAL DIAGNOSIS chap. 

may be of a positive or negative character, e.g. increased knee 
jerk from destruction of brain areas ; or diminished knee jerk from 
irritation of similar areas ; (t>) those which might perhaps be 
more properly spoken of as temporary symptoms, in that they are 
the result of mere increase of pressure which is often capable of 
removal ; examples of which are very common in tumours of the 
brain or pons, and haemorrhage anywhere into the central nervous 
system or its containing cavity. These pressure symptoms must be 
allowed to subside in acute (hsemorrhagic probably, or inflammatory) 
lesions before an exact diagnosis is possible ; and in more chronic 
cases of tumour their possible presence and significance must be 
very carefully considered. 



Incoordination 

For every movement, whether voluntary or reflex, at least two (and 
often many more) muscles or groups of muscle fibres are called into 
action ; and in order that the movement may be co-ordinated 
these several muscles must all act in harmonious relationship to 
each other (i) in time, (2) in amount, i.e. if one of the muscles con- 
cerned acts out of its turn, or with a force disproportionate to that 
exerted by the other muscles concerned, the movement will become 
disorderly, inco-ordinate, and even perhaps inadequate to its avowed 
object. Now, by arguments which cannot be introduced here, it is 
proved that afferent impulses from the muscles to the cerebrum and 
cerebellum (not necessarily, and in fact not usually, causing a con- 
scious perception) are as important for co-ordination as are the 
motor or efferent impulses to the muscles ; and in fact clinical 
experience almost allows the deduction that if inco-ordination of 
voluntary movement be present there is a lesion of afferent tracts 
either of the ordinary class or of the special senses ; disseminated 
sclerosis being almost the only exception, and even here it is 
assumed rather than proved that the inco-ordination arises from 
delay in the transmission of motor, and not afferent impulses. It is 
more commonly complained of in walking (giddiness or stumbling) 
than in other actions, because this requires very complicated and 
delicate adjustments of very many muscles, but clinical examination 
very frequently reveals much that is not complained of by the 
patient. The following are the principal clinical causes of inco- 
ordination, and the leading indications pointing to the probable 
diagnosis. 



DISEASES OF THE NERVOUS SYSTEM 



269 



Cause. 
Peripheral neuritis. 



Affections of pos- 
terior columns 
(? of antero-lateral 
ascending tracts 
too). 

Cerebellar or cere- 
bral disease. 



False optical impres- 
sions. 



Alcohol or other 
general action on 
the sensorium. 



Leading Features. 

"Pins and needles," and other sensation abnormali- 
ties and weakness complained of; skin dystrophy 
or anaesthetic patches ; knee jerks increased or 
absent ; inco-ordination made worse by closing 
the eyes. 

History of lightning pains ; knee jerks absent ; 
inco-ordination worse on closing the eyes. 



Very possibly severe headaches or optic neuritis 
if a tumour ; if other trouble of chronic nature 
history clears up the cause ; closure of eyes 
not likely to make matters worse, because inco- 
ordination is central. 

A squint, found by appropriate tests ; inco-ordina- 
tion improved by closure of the affected eye, 
or of one if both are affected, because this at 
once stops the wrong perceptions. 

History generally obvious ; there are also mental 
alterations, marked in directions other than 
that of co-ordination of movement ; effect of 
closure of eyes variable. 



Reaction of Degeneration 

By' this term is understood those peculiar changes in the elec- 
trical reactions of a muscle which are produced in it by the death of 
the peripheral neurons distributed to it. They are of two kinds — 
quantitative and qualitative. The essential points to be remembered 
about R.D. are: — 

1. It is a phenomenon of muscle only (nerves simply lose irri- 

tability rapidly after severance from their nutritive cells). 

2. It always indicates that the peripheral neuron going to the 

muscle fibre is dead or dying. 

3. It is a phenomenon exhibited by each muscle fibril, and 

consequently is only exhibited in a simple and typical 
manner when at least a large majority of the individual 
neurons going to a gross anatomical muscle are affected ; 
thus is explained its common absence in typical form in 
some cases of progressive muscular atrophy, and other 
slowly progressive neuron destructions. 



270 DIFFERENTIAL DIAGNOSIS chap. 

4. The quantitative element may be thus represented : — 

1st Period. 2nd Period. 3rd Period. 4th Period. 

C - C normal or+ C++ C-o 

F - F - F - o F-o 

where C and F represent irritability to the constant and 
Faradic currents respectively, and period roughly represents 
a week or ten days or less. 
The qualitative element is that — 



The natural 

order of ..O.C. 

.C. 



fK.CC. 
J A.C.C. 
1 A.O. 

[k.o. 



becomes 




during the first two or three periods, but when C and F 
both become diminished — as between the 3rd and 4th 
periods — the above change may occur without our being 
able to make the definite statement that R.D. is present. 



Section II. — Diseases of Nervous System 

Proceeding now to consider pathological diagnosis, it will conduce 
to clearer views of analysis if we insert a — 

Tabular View of the Causes of Diseases of the 
Nervous System 

1 . Traumatism. 

Recent. History obvious. 

Past. May lead to secondary changes of sclerosing or neo- 

plastic nature. 

2. Vascular Disturbances^ with Probable Post-Mortem Eviaence. 

A. Inflammation. 1 

(1) Primary of nerve ^ _, ... 

v ' . f v, I Cerebntis. 

structures, with I ,, ,. . 

., , > Myelitis of cord. 

rapid degenera- [ ' . . .. ... 

.. j 2. ■ 1 Neuritis, poliomyelitis, etc. 

tion and softening. ) r J ' 

1 The terra " inflammation" is used here as the most convenient, because long- 
established, to express the fact ol an acute and very rapid destructive degeneration 
of neuron cells or processes, or both, which may, however, and often does, occur with- 
out very obvious changes in the blood-vessels of the area. 



DISEASES OF THE NERVOUS SYSTEM 



271 



(2) Primary of intersti- 
tial or meningeal 
origin, extending 
to nerve struc- 
tures. 



Meningitis. 
Perineuritis. 



Vascular degeneration. 
Aneurysms. 
Septic arteritis. 

From cardiac valves, aorta, etc. 
From endarteritis obliterans, 
syphilis, tubercle, etc. 



All primarily irritants, and later 
destructive by pressure or by 
invasion of nerve fibres. 



B. Haemorrhage. 

C. Plugging of a Vessel. i 

(1) Embolic. I 

(2) Thrombotic. ( 

3. Tumours. 

Malignant, carcinoma and ~ 
sarcoma. 

Simple connective tissue type 

Tubercular. 

Syphilitic. y 

Abscesses, i.e. cysts of inflam- 
matory origin. 

Cysts of non - inflammatory 
origin. 

4. Scleroses. 

Primary. Either of a distinct system, e.g. 

pyramidal tracts, or of quasi- 
accidental patches. 

Secondary. Following destruction or separa- 

tion of processes from the 
neuron cells by any means 
whatever, e.g. lateral sclerosis 
after cerebral destruction. 

5. Nutritional Disturbances. — A group of cases more easily com- 
prehended by the imagination than defined in words. It is usually 
intended to include hysterical and other cases in which recovery is 
(usually) complete and (not unfrequently) very rapid. They probably 
all have as their essential foundation a primary lowering of the vitality 
of a neuron, with loosening of its synapses with other neurons, thus 
interfering with the transmission of impulses. It is obvious that if this 
process goes beyond a mere chemical or molecular disturbance the case 
may soon have to be put in some organic degenerative group. 

Any of these pathological changes may occur anywhere through- 
out the nervous system, but each one has its seat of election, and 
hence, when the locality of a lesion in any case is settled, we are 
often carried very far in the direction of a diagnosis of its nature, 



272 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



and vice versa. The history of the onset is such an important factor 
in the diagnosis of the nature of a nerve lesion as to necessitate 
the insertion of the following table, copied from Sir W. Gowers : — 



Disease. 



Acute 
traumatism. 



Pressure 

and 
growths. 



Onset. 
Sudden, 

few minutes. 
Acute, 

few hours or days. 

Sub-acute, 

one to six weeks. 
Sub-chronic, 

six weeks to six months. 
Chronic, 

over six months. 



Disease. 



Vascular 
lesion. 



- Inflammation. 



Degeneration or 
scleroses. 



An occasional exception may occur, the most important of 
which is the suddenness with which tumours may now and again 
cause symptoms either by haemorrhage taking place into them when 
otherwise quiescent, or by some slight mechanical alteration in the 
relation of parts when tumour is present. 



Section III. — Differential Diagnosis of Nervous Diseases 

With this introductory outline of the structure, functions, and 
general phenomena of the nervous system, and of its disturbances, 
we may proceed to the more specialised differential diagnosis of 
nervous diseases. 

The first point in the precise diagnosis of an apparently nervous 
group of symptoms must be the determination as to whether the 
symptoms are primarily and essentially caused by an actual lesion 
(organic or nutritional — Gowers) of the nervous system, or whether 
they are secondarily, i.e. purely reflexly, connected therewith, due to 
pyrexia, for example, or local disease of other organs. 

To exhaust from this point of view in tabular form the differen- 
tiation of all the varied phenomena of disease would be confusing 
and unpractical, if not even impossible, considering that it is only 
through our nerve structures that we are made conscious of, and 
adapted to, all the variations of our environment, both local and 
general, and that the co-ordinate or harmonious working of each 
and every organ throughout the body is possible. 



DISEASES OF THE NERVOUS SYSTEM 



2 73 



The following table, then, is but the veriest fragment of an outline 
of the subject, inserted more for logical completeness of the ideal 
object of this book than for serious practical utility, though I have 
endeavoured to make it serviceable as well. 



Chronic and Sub-Chronic Symptom Groups 



If Caused by Essential Affection of 
Nervous System. 

Absence of obvious primary 
peripheral local disease ; es- 
pecially examine blood and 
urine and pelvic organs. 
Motor complaints largely in the 
ascendent ; weakness and loss 
of power in limbs or unsteadi- 
ness ; movement or its loss 
rarely associated with pain. 
Sensory complaints often also 
prominent ; usually numbness 
or paresthesias, if painful most 
likely of a neuralgic, i.e. inter- 
mittent and shooting character, 
or without obvious objective 
causation. 

Complaints of vague alterations 
from the usual harmonious ease 
of the acts of micturition and 
defalcation. 



5. Insidious onset, very variable 
progression, and unlimited chro- 
nicity. 



6. Reflexes probably altered. 



If Secondarily or Reflexly Nervous. 

1. Such disease is present; cau- 
tion — secondary trophic lesions 
not to be mistaken for pri- 
mary. 

2. Such complaints absent, except 
with obvious disease of muscles 
or alteration in outline of joints 
or limbs : gout, rheumatism, 
epiphysitis, etc. 

3. Such complaints practically 

only of a painful nature, and 
frequently with obvious causa- 
tion, e.g. chronic pleurisy, cold, 
abscesses, etc. 



Complaints about these acts 
usually of a straightforward 
difficulty in act, or definite 
alteration in frequency, e.g. 
stricture, enlarged prostate, 
etc. 

Onset fairly marked, progress 
more uniform and chronicity 
limited, e.g. rheumatoid arth- 
ritis, chronic Bright's disease, 
etc. 
Reflexes probably unaltered. 



Comments on the Table, and Additional Remarks 

1. The examination of blood and urine are expressly mentioned 
to avoid the mistaking for primary nervous affections the numerous 
vague and obscure secondary phenomena that occur in anaemia and 
other primary blood dyscrasiae, and are the prominent symptoms 
of chronic and even acute uraemia. A careful examination of the 

t 



274 



DIFFERENTIAL DIAGNOSIS 



pelvic organs will often reveal a very substantial cause (neoplasm, 
parametritis, etc.) for a puzzling sciatica. 

2. In children, and even sometimes in adults, it is difficult to 
distinguish between the refusal to move a limb or part because 
such movement causes pain (pseudo-paralysis) and the incapability 
of such movement ; the effect of passive movement painful in the 
former, not in the latter, is the simplest test, and usually sufficient. 
Other cases in which movement causes exaggeration of already 
present pain will be referred to in various places where the fact is of 
use in separating individual complaints. 

Inco-ordination of movements, and tremors on effort, are very 
suggestive of primary nerve lesions, the various forms of Grave's 
disease being the chief fallacy. 

General convulsions and local spasmodic twitchings of muscles 
constitute evidence of such importance as to require separate con- 
sideration. 

Vomiting, if reflex from nerve lesions, is usually paroxysmal, 
very persistent during a paroxysm, and not accompanied by much 
nausea as a rule ; it may be excited by food, but occurs equally 
independent of it {vide p. 158). 

Mental changes, except when accompanied by pyrexia, are 
almost always indicative of an essential nerve lesion, most commonly 
of the nutritional type when the symptom is primary ; when it is 
secondary to some organic destruction its cause is usually fairly 
obvious. 

Wasting, if general, rarely points to organic disease of the 
nervous system ; but if local, it becomes very suggestive of such a 
causation {vide p. 252). 



Acute and Sub-Acute Symptom Groups 



% * 



If Caused by Essential Affection of 
Nervous System. 

f I. Pathological activity, or pos- 
sibly inactivity of nerves 
(headache, pain, spasm, de- 
lirium, etc.), out of propor- 
tion to the degree of fever, 
and not necessarily abating 
with defervescence. 
Rapid onset of actual loss of 
function of nerves — paralysis, 
anaesthesia, etc. 



If Secondarily or Reflexly 
Nervous. 

This activity or its re- 
verse is more or 
less proportional to 
the fever ; usually 
abates with it. 



No paralysis, or if so, 
it is pseudo-paralysis. 



vin DISEASES OF THE NERVOUS SYSTEM 275 

On this tabular differential diagnosis of acute symptom complexes 
it is only necessary to remark that there are but few general points 
that can be utilised for the purpose. In the cases in which the 
greatest difficulties and the most serious mistakes are likely to 
occur the differential points are rather special than general, 
and consequently the diagnosis will be found in special tables ; 
vide — 

Meningitis v. Pneumonia, pp. 95 and 96. 

Tubercular Meningitis v. Gastritis, pp. 159 and 160. 

Infantile Paralysis v. The Exanthemata, p. 292. 

Acute Mania v. Delirium Tremens. 

Organic v. Functional Lesions 

We may now continue with general differential diagnosis, on 
the assumption that the case before us is really and essentially 
nervous. The next point to determine is whether it be organic or 
functional. 

Even in an elementary work it is impossible to avoid glancing 
at a definition of these terms. The difficulties in the way of an 
accurate investigation of the microscopical details of the (whole of 
the) nervous system have hitherto been so great as to practically 
prevent a final decision of the question, " Is the picture of structure 
normal or abnormal, physiological or pathological ? " and then of the 
question, "Did the ill-regulation of function during life depend 
upon the peculiarities of structure which have been noted ? " As 
modern methods of microscopical technique (hardening, preserving, 
staining, etc.) become more and more perfect, we are coming more 
and more to the conclusion that a final answer can be given to the 
first of these questions, and probably, in consequence, to the second, 
so that the field of genuine functional diseases is rapidly becoming 
more and more restricted. 

Theoretically, we can conceive that a piece of living machinery 
that was originally (in congenital troubles the same argument 
applies to the development of structure) capable of carrying out 
its due function properly and in harmony with the functions of 
other nervous complexes may work improperly or inharmoniously 
( = disease) by assuming (1) that its structure has got damaged, or 
(2) that its supply of nutriment is faulty (excessive, inadequate, or 
deleterious), or (3) that it individually is suffering from wrong con- 
trol (imperfect, excessive, or perverted) by other "centres." The 
last two would correspond to functional, the first to structural, 



276 DIFFERENTIAL DIAGNOSIS chap. 

disease ; but it is very easy to see that what was at first purely 
functional, qua a given " centre," may readily result in organic 
destruction if the untoward influences persist. 

As common examples of diseases which are at present frequently 
thought of as functional, and illustrating the above theory, I would 
mention — 

Epilepsy. — Due primarily to a fine (some day, I believe, to be 
definitely described) organic change in structure of a centre or 
centres, kept up or made worse by improper nutriment. Witness 
the bad influence of some diets (meat) on epileptics. 

Hysteria and Neurasthenia. — Due primarily to imperfect nutrition 
of higher centres, and then a consequent loss of control of these over 
lower centres which exhibit the symptoms. (Some cases are very 
close to deliberate malingering.) 

Neuralgias. — Often due to organic (inflammatory) changes, but 
strictly to improper nutrition. 

Delirium and other Phenomena of Fevers and of Apyrexial Toxaemia. 
— Due at once and essentially to deleterious substances supplied to 
the nerve, often ending in definite structural trouble. (Witness 
diphtheria, influenza, etc.) 

Manias and Permanent Mental Obliquities. — In causation closely 
allied to the temporary troubles of fevers, etc. ; but more frequently 
the cause ends in fine microscopical changes, which are already being 
investigated with success. 

Occupation Neuroses. — Essentially due to overwork, which in turn 
leads to, or is associated with, imperfect nutrition by excess of 
waste products. (These cases are very often ones of definite 
neuritis.) 

Minor Symptoms of Diseases of Brain. — Are in themselves nothing 
but functional, and are illustrations of perverted control. Typical 
examples are alteration of reflexes, disturbances of visceral functions, 
etc. 

Considering the very small capability of repair possessed by the 
nervous system when once a cell has been damaged, it would seem 
almost sufficient to define organic as that which is incapable, 
functional as that which is capable, of repair. Excepting inflamma- 
tory troubles, this is very nearly my meaning in what follows. 

Most commonly the point will be obvious from the general 
aspect and history of the patient, but in cases of doubt the follow- 
ing table will assist us : — 



VIII 



DISEASES OF THE NERVOUS SYSTEM 



277 



Organic. 
Onset. 

If sudden, usually the symptoms 
are fairly definite and local- 
ising. 
If chronic, it is still usually fairly 
constant in character, and con- 
sistent in progress. 

Motor Symptoms. 

Paralysis. — Far and away the 
most common result ; if flaccid 
it is rapidly followed by R.D. ; 
in all cases its distribution is 
in accordance with known 
anatomical structure, and ob- 
jective signs may frequently 
be found when due to lower 
level lesions ; constant in posi- 
tion when once apparent, at 
least does not dodge from 
limb to limb ; may be incom- 
plete. 

Spasm. — Rarely due to organic 
lesion except in Jacksonian 
epilepsy and the convulsions 
of meningitis ; may occur 
during sleep ; when organic 
usually a definite known causa- 
tion in history. 

Sensory Symptoms. 

Not common as the sole com- 
plaint ; if it is the only com- 
plaint it is usually definite and 
localising. 



Reflexes. 

Experimental. — Most usually 
definitely and permanently 
altered, and in a constant 
direction for the individual 
case. 



Functional. 

If sudden, it is less definitely local- 
ising, and symptoms more vague, 
frequently prominently mental. 

If chronic, it is very inconstant in 
features, and inconsistent in pro- 
gress. 

Also tolerably common, but even if 
flaccid, R.D. never develops ; in 
most cases it is apparently due 
to lower level lesion, and yet no 
objective signs to be found ; its 
distribution varies from time to 
time ; usually complete in the 
member complained of. 



Very common; usually ceases during 
sleep ; no ascertainable cause in 
the history. 



Often enough the sole complaint, 
indefinite and non - localising ; 
definite hemianesthesia will be 
unassociated with any features 
pointing to organic brain trouble, 
e.g. hemiplegia or unconscious- 
ness at onset. 



Variable in different cases which 
are otherwise similar, and also 
in the same case from day to 
day. 



278 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



Organic. 

Visceral. — Micturition and defae- 
cation often seriously affected, 
as also many other visceral 
functions. 

Vascular. — Often loss of vaso- 
motor control, limbs cold, and 
circulation too easily influ- 
enced by local conditions ; 
may cause serious anxiety. 

Mental Changes. 

When present usually persistent, 
and are associated with other 
definite indications of organic 
trouble. 

Total Aspect and Course. 
Constant. 
Consistent. 
Definite. 



Functional. 
Rarely or never serious visceral 
mischief, but there may be 
troublesome retention of urine. 

Such loss of control only shows 
itself in turgescent directions 
(factitious urticaria, e.g. ), or very 
temporary coldness and white- 
ness ; never looks serious. 



Characteristically variable, and 
present before illness, or at least 
not directly caused by it ; unas- 
sociated with other definitive in- 
dications. 



Inconstant. 

Inconsistent. 

Indefinite. 



The mimicry of organic disease by functional changes is, how- 
ever, sometimes so complete and so intricate that further details 
can only be given in special cases. 

Assuming that we have determined the case to be one of organic 
disease, one of the first questions that requires an answer will be — 
"Is it of the brain or encephalic structures, or is it of the cord (in- 
cluding medulla) or periphery ? " 

The clearest method of reply is to divide all cases into two 
categories: (1) acute, a week or less; (2) chronic, a month or 
over. 



A. — Acute Nervous Lesions 

Before deciding as to an apparently acute case it is exceedingly 
important to make inquiries into the previous history of the patient, 
because the following acute incidents in chronic diseases may mis- 
lead us : — 

Fits in epilepsy. 

„ general paralysis of the insane. 

„ chronic poisoning (alcohol, lead, etc.). 

„ cerebral tumours. 



DISEASES OF THE NERVOUS SYSTEM 



279 



Crises in tabes dorsalis. 

Acute features in chronic spinal caries. 

„ „ ear disease, etc. 

„ „ meningitis. 

Excluding such cases, the following points are most important : — 
t_i. • 1 Cord and some Peri- 



Onset. 



Consciousness. 



Motor Symptoms. 
Cranial Netves. 



Intracranial. 

Very sudden onset is 
extremely common. 

Very often interfered 
with in some degree. 

Often implicated in 
some degree. 



Paralysis or paresis Almost invariably on 
or excessive move- one side ; if on both, 
ment. nearly sure to be 

much interference 
with consciousness 
or with cranial 
nerves, as in ven- 
tricularhsemorrhage 
or pontine lesions. 



Sensory Symptoms. 



Reflexes. 



Comparatively rare 
alone ; if present, 
they are of the hemi- 
type. 



Of eye frequently lost. 



Knee jerk frequently 
altered on one side 



Cord and some Peri- 
pheral Lesions. 

Such suddenness is 
rare. 

Practically never inter- 
fered with. 

Rarely or never impli- 
cated, unless it be 
as regards the dila- 
tion of pupil, and 
in post - diphtheritic 
paralysis. 

Almost invariably on 
both sides, owing to 
nearness of the two 
sides in the cord, 
and to the sym- 
metry of peripheral 
nerves in liability to 
poisoning ; area of 
disturbance very 
small if one-sided. 

Very common indeed, 
and of the para- 
type; because 
motor and sensory 
tracts are so close 
together in cord, and 
both have a nearly 
equal tendency to 
suffer in poisoning 
(? except diphtheria). 

Of eye lost sometimes 
in lesions high up 
in cord. 

Frequently altered, but 
more probably on 



280 



DIFFERENTIAL DIAGNOSIS 



CHAP. 



Intracranial. 

only, unless great 
excess of intracra- 
nial pressure. 

Bladder and rectum 
rarely affected, un- 
less consciousness 
is much interfered 
with. 



Cord and some Peri- 
pheral Lesions, 
both sides, and that 
without evidence of 
intracranial pres- 
sure. 
Bladder and rectum 
often interfered with 
in acute cord lesions, 
and that without 
interference with 
mental clearness. 



If the case be a less acute one (over a month), and seems to be 
stationary or progressing, the following table may be constructed : — 

B. — Chronic Nerve Lesions 



Intracranial. i 

History. 

More frequently a history of 
an acute attack or attacks, 
and if such be the case, 
symptoms very possibly 
stationary or improving ; 
tumours the great excep- 
tion. 
Motor Symptoms. 

Jacksonian epilepsy (q.v.) 
common enough. 

One side most likely alone 

affected. 
Cranial motor nerves often 

affected. 



Sensory Symptoms. 

Again one-sided and cranial ; 
" pins and needles," and 
other paraesthesiae, if pre- 
sent, are of one arm or leg, 
or one side. 



Extracranial. 

Less frequently such history with 
stationary symptoms ; the symp- 
toms are likely to be progressing, 
except in cases of definite myelitis. 



Such uncontrollable movements only 
take the shape of twitching in legs 
or arms. 

Both sides most often affected. 

Cranial nerves rarely affected except 
in disseminated sclerosis and in 
tabes dorsalis, in both of which the 
lesion may extend to encephalic 
centres. 

Both sides, and not cranial ; " pins 
and needles," if symmetrical, almost 
pathognomonic of a peripheral 
lesion ; sensory disturbances in cord 
troubles nearly sure to be acutely 
painful or completely anaesthetic. 



vin DISEASES OF THE NERVOUS SYSTEM 281 

Intracranial. v. Extracranial. 

Reflexes. 

Often one-sided change ; if Equally affected, and that without 
both sides, nearly certain mental symptoms, 

to have cranial nerves 
affected, or mental symp- 
toms. 
Mental Changes 

Common. Never present in a purely cordal 

lesion, or in one of peripheral 
nerves. 

It is impossible to pursue the plan of general tables for differ- 
ential diagnosis farther, owing to the mass of details necessary for 
complete diagnosis, which would be quite irrelevant in many in- 
dividual diseases. We must now proceed to consider the separate 
affections, with tables to differentiate those which are more nearly 
similar. 

Peripheral Neuritis 

The existence of lesions of the peripheral nerves, independent 
of trouble in the cord and brain, has only been determined within 
quite a recent period ; consequently, the first and commonest diffi- 
culty in their diagnosis arises from a want of familiarity, not with 
cases of the disease itself, for they are only too frequent, but with 
the idea of its existence ; and non-acquaintance has, as its natural 
corollary, non-recognition. It may be laid down as a law that — 

"In the gross total of nervous diseases peripheral neuritis, in 
some one of its many forms, is exceedingly common, and its possible 
presence must always be borne in mind." 

Now, how — in what connections — does it occur, and what are 
its prominent features ? As far as diagnosis is concerned, it occurs 
in two fairly distinct forms : — 

(a) More or less localised to individual-named nerves and their 
branches ; a search along which will often reveal the cause of the 
trouble, e.g. a septic wound or tumour causing pressure, though it 
must not be forgotten that general constitutional poisons, such as 
rheumatism, gout, or lead, may, and often do, produce such local 
asymmetrical affections. 

(fr) More universal affection of a large number of nerves 
(multiple neuritis of authors), almost invariably due to a poison 
carried by the blood, e.g. alcohol, etc., and almost invariably sym- 
metrical. 



282 DIFFERENTIAL DIAGNOSIS chap. 

It is rather a peculiarity of peripheral nerve troubles that they 
are often either of sensory or of motor nerves only, a point apt to 
be overlooked ; but mixed cases, both sensory and motor, are per- 
haps more commonly met with. The prominent symptoms are the 
following : — 

i. Motor Side. — Weakness and wasting of muscles, with flaccid 
paralysis, and possibly R.D. ; certainly R.D. if the case is severe, 
because the peripheral neuron is the main channel by which nutri- 
tion of terminal organs is maintained. 

2. Sensory Side. — The inflammation acts as an irritant of the 
peripheral sensory neuron, possibly proceeding even to complete 
destruction of function ; hence we get — 

(a) " Pins and needles " and numbness. If these are well marked 

and persistent, and on both sides, they are almost, if not 
quite, pathognomonic of a peripheral lesion. 

(b) Pain and hyperaesthesia in the known area of distribution 

of certain sensory nerves. 

(c) Anaesthetic patches. These require to be looked for, as 

the patient has very probably not appreciated their pre- 
sence. Possibly these anaesthetic regions or areas may 
be the alleged seat of painful sensations — paradoxical or 
painful anaesthesia. 

3. Reflex Side. — Experimental reflexes, especially the knee 
jerk, either grossly exaggerated (in early stages), or more probably 
absent ; visceral reflexes are almost universally unaffected, so that 
serious disturbance of micturition or defaecation is practically con- 
clusive proof that the cord or brain is affected. 

4. Trophic Side. — Muscles waste rapidly {vide Motor Side) ; the 
skin and its appendages show very characteristic appearances ; nails 
become brittle and crack very readily ; hair falls out or is tempor- 
arily excessive in growth ; skin becomes very smooth, shiny, and 
thin. 

5. Cranial nerves may be affected, but if so, entirely without 
general symptoms, and also without any pathological mental pheno- 
mena. 

If, then, in a given patient some or many of the above are 
present, we must suspect a peripheral lesion, and inquiry or volun- 
teered statements may then very likely reveal the presence of some 
antecedent condition known either to predispose or to excite such 
changes. These, with the leading feature of the resultant neuritis, 
are given in the following table in rough order of frequency. 



DISEASES OF THE NERVOUS SYSTEM 



283 



Clinical Causes of Peripheral Neuritis 



Injury, including local in- 
flammation and pressure ; 
septic wounds ; necrosis of 
bone, syphilitic, tubercular, 
cancerous, aneurysmal, etc., 
tumours ; probably as a 
sub-group come occupation 
neuroses (often neuritis). 

Diphtheria. 



Causation obtrusive ; only the pain or 
paralysis, or both, make one say 
neuritis is present ; the case is 
named from the causation, and not 
necessarily called neuritis. 



3. Rheumatism and gout. 



Alcohol (with this, but in- 
finitely rarer, must be put 
poisoning by CS 2 , aniline, 
and a few other trade 
products). 



Symptoms almost entirely motor, and 
especially of the eye and palate, 
but knee jerks almost invariably 
absent. 

Almost entirely sensory, and pain in 
the course of a nerve, with a history 
of gout or rheumatism, the chief 
guides. 

Both sensory and motor ; here " pins 
and needles" is a very constant 
feature, with progressive weakness 
in legs and arms ; history of alcohol 
(possibly denied) or of trade occu- 
pation. 

As a peripheral nerve trouble, usually 
confined to wrist drop, and colic 
(? nervous) ; blue line on gums is 
the guiding feature. 

Sensory and motor, usually preceded 
or accompanied by coryzal symp- 
toms. 

Glycosuria ; mainly neuralgic symp- 
toms in a given nerve ; also absence 
of knee jerks. 

8. Cases occurring in the course of the exanthemata, which present no 

special diagnostic points ; also in anaemia and other cachectic 
conditions, e.g. senility. 

9. Malaria, leprosy, beri-beri, and other tropical forms too rare in 

England to require further notice here. 

The presence of one or more of these causes will then often go 
far towards clinching the diagnosis. Cases will, however, often 
enough occur in which the cause is not obvious — overlooked, 
denied, or forgotten — and we may have to depend on the symptoms 
alone for a diagnosis. 



5. Lead. 



Arsenic. 



7. Diabetes. 



284 



DIFFERENTIAL DIAGNOSIS 



For what affections can the symptoms of peripheral neuritis be 
mistaken ? Simple neuralgia and affections of the cord and brain 
are the ones chiefly requiring distinction. 

Neuritis v. Neuralgia 

I have adopted the word " neuralgia " here to indicate a pain not 
due to gross organic changes in a nerve, for the diagnostic problem 
I wish to try to solve is the following : Is this pain complained of 
by the patient a purely reflex phenomenon, or at least only due to 
nutritional (so-called functional) changes, or is it due to gross organic 
changes, of which actual neuritis is our present example? The 
following table gives the main points of difference : — 



Table 



Reflex or Functional, i.e. Neuralgia. 

More likely to be paroxysmal in 
character. 

Spontaneous in onset, independent 
of use of nerve, and, in fact, 
often better during bodily activ- 
ity 

Intermittency complete, and history 
may show long intervals of in- 
termittency. 

Situation often variable from day 
to day, but almost invariably 
unilateral in any given attack. 

If points douleureux present, which 
they rarely are, pressure on them 
causes pain at the periphery. 

Little or no local tenderness along 
nerve trunk, and especially a 
light pressure will cause as much 
pain as a heavier one. 

Wasting or other trophic dis- 
turbances never present at first, 
and only rarely after a long 
time. 



Organic, i.e. Neuritis. 
Less likely to be of this character. 

Pain usually excited by movement, 
often subsides when a posture 
of rest adopted, and always 
worse after use. 

If intermittent, rarely completely 
so, and not for long. 

Situation never variable from day 
to day ; more commonly bilateral, 
but may be either. 

Points douleureux usually present, 
and pressure on them causes 
very distinct local pain, as well 
as perhaps peripheral. 

Generally local tenderness along 
nerve trunk, and pain much 
more proportional to amount of 
pressure. 

Wasting and trophic disturbances 
nearly certain to appear rapidly, 
and may even proceed to R.D. 
in muscles. 



Some of these points can be investigated with a definite result 
in any stage of the malady, but for others time must be allowed, 
and often in the early days of symptoms a definite diagnosis is 



vin DISEASES OF THE NERVOUS SYSTEM 285 

impossible ; but if the cause be organic the nerve is almost sure in 
a very short time to show very definite signs of loss of function and 
degeneration, whereas a reflex or functional pain may continue for 
years without such signs. 

To avoid needless repetition, the further distinction between peri- 
pheral neuritis and cord troubles can be better discussed after we 
have considered an outline of the functions and affections of the cord. 



DISEASES OF THE SPINAL CORD 

Of the real exciting causes of primary affections of the spinal 
cord we know very little, indeed practically nothing. This is in 
great contrast to our knowledge of causes of peripheral troubles, 
but traumatism (external and internal), tumours, acute inflamma- 
tion, and a slowly destructive process — ultimately ending in de- 
generation of neurons and a condition known as sclerosis — are the 
chief clinical causes of those pathological symptoms which we 
discover by examination. It must be accepted as a fact that the 
last-mentioned cause (and often also acute inflammation) has, to an 
extraordinary degree, a habit or power of attacking parts of the 
spinal cord possessing analogous function, and symmetrically situated 
on either side of the middle line. So constantly is this the case 
that these affections are now spoken of as system diseases in 
opposition to the indiscriminate lesions produced by tumours, 
haemorrhages, etc. 

System Lesions of Spinal Cord 

The systems thus picked out are : — 

1. The cells of the anterior cornua ; 

2. The fibres of the pyramidal tracts (crossed and direct) ; 

3. The fibres of the posterior columns ; 

and the names given to the diseases thus produced may usefully 
be tabulated as follows : — 
Anterior Cornua — 

p . j Chronic = Progressive muscular atrophy. 

^ ( Acute = Infantile (or adult) spinal paralysis. 
Secondary to acute = Myelitis or tumour pressure, etc. 
Lateral Columns 
or Pyramidal 
Tracts — 

Primary = Primary lateral sclerosis or spastic para- 

plegia. 



286 DIFFERENTIAL DIAGNOSIS chap. 

Secondary * = Secondary spastic paraplegia, caused by 

any destruction of the nutritive cells in 
the rolandic cortex, or by division or 
destruction of the main neuron stems 
from them, such as is left by an acute 
transverse myelitis. 
Posterior Columns — 

Primary = Tabes dorsalis or locomotor ataxy. 

Secondary = Acute myelitis or tumour pressure, etc. 

Besides these pure or simple lesions we have two named com- 
binations — 

Combination of anterior cornua and = Amyotrophic lateral sclerosis. 

pyramidal tracts. 
Combination of pyramidal tracts = Ataxic paraplegia. 

and posterior columns. 

The diseases in the right-hand column form then the labels of 
the system lesions of the cord. With the exception of acute anterior 
poliomyelitis they are all, when primary, i.e. without obvious cause, 
chronic in onset (a year or more). After or during an indiscrimi- 
nate lesion (tumour, haemorrhage or softening, traumatism, acute 
myelitis, all of which except tumour are acute or sub-acute in onset) 
the symptoms of the system lesion constitute the evidence of loca- 
tion vertically and horizontally. We will now proceed then to tabu- 
late the known functions of the systems to get a firm foundation for 
differential diagnosis : — 

Table 

Functions of Systems of Cord 

Pyramidal Tracts. Anterior Cornua. Posterior Columns. 

Motor Telegraph wires Receive by their Nil. 

conveying dendrites 

motor mes- motor mes- 

from cells sages from 



of rolandic cor- pyramidal 

tex to dendrites tracts. 
of cells of an- 
terior cornua. 

1 This is not usually named as a separate disease, but a symptom-complex or 
residual condition produced by or left after the lesions mentioned — tumour, haemor- 
rhage, inflammation, etc. 



DISEASES OF THE NERVOUS SYSTEM 



287 



Sensory. 



Reflex. 



Trophic. 



Pyramidal Tracts. 
Nil. 



Transmit im- 
pulses from the 
brain having a 
restraining in- 
fluence on 
spinal reflexes. 

Nil. 



Anterior Cornua. 
Nil. 



Form a link in the 
reflex chain for 
any given level. 



Forms the main 
source of tro- 
phic influences 
for the peri- 
pheral neuron 
and for the 
muscles. 



Posterior Columns. 

Sensory telegraph 
wires convey- 
ing messages 
from skin, 
muscles, etc., 
up to medulla 
and brain. 

Also form a link 
in the chain at 
a given level. 



Possibly transmit 
trophic influ- 
ences to skin. 



The Consequent Symptoms of Irritation or Destruction of the Systems are 
Pyramidal Tracts. Anterior Cornua. Posterior Columns. 



Motor. 
* At the 
seat of 
lesion. 



* Below the 
seat of 
lesion. 



Movements or 
paralysis cor- 
responding to 
the fibres going 
out at the level. 

Movements or 
paralysis pro- 
portional in 
extent to the 
number of 
fibres d e- 
stroyed, hence 
may be merely 
general weak- 
ness ; paralysis 
not flaccid. 



Paralysis flaccid, ] 
and with R.D. 
in muscles. 



No influence on 
lower cells and 
muscles. 



Inco - ordination 
without loss of 
power; due to 
interruption of 
afferent im- 
pulses from 
muscle by the 
sensory nerves 
to the encepha- 
lon or head co- 
ordinating 
centre; no para- 
lysis or convul- 
s i v e move- 
ments. 



* The reason for the difference in symptoms at the seat of lesion, and above and 
below it, should be most carefully noted. It is that the posterior columns and the 
pyramidal tracts are merely bundles of telegraph wires, the vast majority of which 



288 



Sensory. 
* At the 
seat. 



DIFFERENTIAL DIAGNOSIS chap. 

Pyramidal Tracts. Anterior Cornua. Posterior Columns. 



Nil. 



* Below the Nil. 
sea' 



Nil 



Nil. 



Root pains pos- 
sibly, girdle 
sensation. 

Anaesthesia of 
opposite side 
proportional to 
the number of 
fibres de- 
stroyed ; pains 
possible from 
irritation of un- 
destroyed 
fibres. 



Reflexes A of Experimental Production. 



* A t the Absent knee jerk Absent from break Absent from break 
seat. in destructive in chain. in chain. 

lesions from 
break in chain. 

* Below the Increased from 

seat. absence of re- 

straint in de- 
s t r u c t i v e 
lesions ; in irri- 
tative lesions 
knee jerk is 
variable. 

are in any given section of the cord merely passing through the seat of section, con- 
ducting impulses which actually exhibit themselves lower down or higher up as motion 
or perception ; it is only a very few that at any point leave the cord as the direct con- 
tinuation of a peripheral neuron with incoming or outgoing message. The reverse is 
the case with the cells of the anterior cornua, which are all of them in any section 
individually in relationship with peripheral neurons proceeding from that plane of 
section (or at least from very closely situated planes) ; they have no serial functional 
relationships (of clinical utility at present at any rate) with more distant cells above 
and below. A similar, I might almost say the same, explanation may be given of 
the term "root symptoms," an expression frequently used in nervous clinical patho- 
logy. It means symptoms, motor or sensory, which can be traced to irritation 
(usually), or destruction of the peripheral neurons constituting a motor or sensory root 
of a spinal nerve, either just outside the cord or just within it (after they have left the 
cells of the anterior cornua in motor cases, before they have been separated in the 
posterior columns in sensory cases), but leaving the cord at that plane; they will 
obviously be segmental in distribution, i.e. a girdle pain or a local pain in the back 
corresponding to the sensory nerve, or, on the other hand, a twitching or paralysis 
and atrophy of certain muscles corresponding to named motor nerves. 



DISEASES OF THE NERVOUS SYSTEM 



289 



B of Viscera. 



Pyramidal Tracts. Anterior Cornua. Posterior Columns. 



No voluntary as- 
sistance to the 
act possible, 
but the centres 
may work har- 
moniously. 



Loss of expulsive No consciousness 



Trophic to Skin and Muscles. 

*At the No effect, because 
seat. peripheral neu- 

ron unaffected. 



* Below. Nq effect. 



or containing 
power if in 
lumbar region, 
and so drib- 
bling or reten- 
tion of urine ; 
in regions other 
than the lum- 
bar result on vis- 
cera unknown. 

Rapid wasting, 
with R.D. of 
muscle fibres 
or whole 
muscles, cor- 
responding to 
destroyed cells. 

No effect. 



of acts, and 
great mischief 
may ensue if 
centres do not 
work harmoni- 
ously. 



Bed sores not in- 
frequent, either 
from anaes- 
thesia or 
absence of 
usual trophic 
influences. 

Same as at the 
seat. 

In addition to these three systems we have clinical evidence 
that the antero-lateral ascending tract of Gowers conveys impres- 
sions of pain and touch to the sensorium, and that the gray matter 
has, amongst other functions, the power of conveying impressions of 
changes of temperature to the brain, and probably also of control- 
ling the nutrition of the skin and sub-cutaneous structures. Sir W. 
Gowers has brought forward much evidence in favour of the first pro- 
position j the known thermal anaesthesia of syringomyelia is sugges 
tive of the correctness of the second ; and the third is one possible 
explanation of the rapid development of bed sores in acute myelitis. 

These tables show very distinctly that if a system disease be 
present in a typical form confusion is impossible, for their symptoms 
present positive contrasts rather than comparisons. The combined 
chronic lesions are rather more confusing, and it is moreover true 
that atypical and indiscriminate lesions are frequent, and hence the 
differential diagnosis requires some little discussion. 

The first caution and golden rule is, " Don't be in a hurry to make 
a final and definite diagnosis, to find, as it were, a ready-made label 
* See footnote, pp. 287-288. 
U 



290 DIFFERENTIAL DIAGNOSIS chap. 

for a case." Consider well the absence as well as the presence of posi- 
tive symptoms, and then let the diagnosis run, " From what I have 
observed, I have reason to believe that such and such parts of the 
cord are affected, and, owing to the absence of certain features, 
other parts are exempt." If the case be typical the appropriate 
label will then be found, and if atypical no opinion will have been 
expressed which may afterwards have to be withdrawn. 

Indiscriminate Lesions 

Inasmuch as an indiscriminate lesion of the cord can only be 
diagnosed, so far as its symptoms are concerned, by its effects upon 
those systems or parts of the cord with the functions of which we 
are more or less acquainted, i.e. by the same phenomena — motor, 
sensory, reflex, and trophic — already several times noted, there 
follow as immediate and necessary deductions (i) that the history 
of onset of the illness, and the grouping of the signs, will be of much 
more importance than their individual presence; (2) that the 
vertical or horizontal localisation will also assume an equal impor- 
tance to ascertain if local therapeutical measures offer a prospect of 
radical cure, e.g. tumours. 

The lesions themselves are practically only three, viz. trauma- 
tism, vascular lesions (blocking, rupture, or inflammatory), and 
tumours, though syringomyelia and disseminated sclerosis ought 
also to be enumerated if they had not such special characteristics 
of their own. 

They all of them cause either irritation followed by destruction, 
or immediate destruction of the cord, and may be classified from 
that point of view as follows : — 

A. Irritative period Meningitis, simple chronic. 

long, weeks or Tertiary gummata and other tumours of 

months, or even meninges. 

years. Aneurysmal erosion of bone and compression. 

Spinal caries when products cheesy and possess 
but feeble potency of irritation, or when gradual 
bone displacement causes pressure. 
Tumour of the bones. 

Traumatism that has only excited slight inflam- 
matory changes. 

B. Irritative period Spinal caries with suppuration or sudden displace- 

short : hours or ment of bone. 

days. Syphilis within two years of infection. 



DISEASES OF THE NERVOUS SYSTEM 



291 



C. Irritative period 
almost non-ex- 
istent. 



Tumours of any origin (occasionally). 

Meningitis, acute general. 

Meningeal haemorrhage. 

Acute myelitis (this often occurs in cases where 
longer irritative period might be looked for, 
e.g. acute meningeal inflammatory affections). 

Haemorrhage into cord, or softening from blocking 
of a vessel. 

Traumatism when severe. 

Hence it is obvious that it is hardly possible to mistake any of 
the members of Groups B and C for a system lesion (except 
perhaps acute infantile paralysis), the history of the onset of the 
symptoms stands in such absolute contrast. The cases of Group A, 
too, are almost invariably characterised by one distressing symptom, 
which is as invariably absent from system lesions, viz. severe local 
pain or tenderness in the back, a root symptom {q.v., p. 288, foot- 
note). 

Besides these two fundamental differences I only propose to give 
the following brief notes on the diagnosis of indiscriminate lesions. 

TRAUMATISM. A definite history of some violence always to be 

obtained ; in slight cases interference with mic- 
turition is the most suspicious circumstance, 
suggesting serious cord trouble ; a chronic 
meningitis or myelitis may arise from this 
cause analogous to concussion of brain. 

Exceedingly rare, onset instantaneous, consequent 
and subsequent symptoms those of an acute 
myelitis, unless the clot or area of softening be 
very small, when they will be those of a system 
lesion, only of acute origin, and probably 
asymmetrical. 

Also excessively rare except from traumatism or 
ruptured aneurysm, in each of which diagnosis 
is obvious ; if a small meningeal haemorrhage 
were met with it would be indistinguishable 
from localised meningitis or tumour except by 
very sudden onset. 

Focal or root symptoms very prominent ; com- 
plete symptoms more rapid in onset than 
sclerosis, less so than inflammation ; jumpings 
of a limb with pain in it for some months prin- 
cipal characteristics from pressure on posterior 
or lateral tracts. 



H MM ORRHAGE 
INTO OR SOFTEN- 
ING OF CORD. 



HEMORRHAGE 
INTO MENINGES. 



Tumour of menin- 
ges. 



292 DIFFERENTIAL DIAGNOSIS chap. 

TUMOUR OF SUB- Very rare ; symptoms similar to meningeal tumour, 
STANCE OF THE but much more rapidly progress towards a 

CORD. paralytic as opposed to an irritative aspect. 

System Lesions v. Peripheral Neuritis 
We may now return to peripheral neuritis and those affections 
of the cord for w r hich it may be mistaken. There are two systems 
of the cord, disease of which can obviously cause mistakes, viz. the 
anterior cotnua (motor) and the posterior columns (sensory), and 
that because anterior poliomyelitis and tabes dorsalis are, in fact, 
lesions of the same peripheral neuron as motor and sensory peri- 
pheral neuritis respectively. 

Pathologically the difference lies in the exact point in the 
neuron where the trouble begins. This is in the cells of the 
anterior cornua, and of the posterior roots l in the system lesions, 
with consequent rapid secondary degeneration of neuraxons. While 
in peripheral neuritis the affection, if not limited to the neuraxon, 
at least begins in it, and only secondarily involves the neuron cell 
in severe cases. Clinically we are fortunately able to find a good 
many differences, so that in the majority of cases but little difficulty 
arises in diagnosis ; though it must be confessed that often also only 
time and very great patience will but partially unravel the mystery. 

A. — The Onset 
The onset of the system lesions is, as a rule, in marked contrast 
to that of the peripheral troubles. 

Anterior poliomyelitis occurs as : — 

i. Acute, (a) Idiopathic infantile paralysis. 
{b) „ adult „ 

(c) Part of an acute myelitis. 
2. Chronic, or progressive muscular atrophy. 
Sclerosis of the posterior columns is, as an idiopathic affection, 
always chronic. 

Now, acute infantile paralysis commences with a sharp outburst 
of fever, and cannot be diagnosed from a zymotic fever until its 
special symptom, viz. paralysis, has supervened. Inasmuch as there 
is a concomitant congestion of the spinal cord, this onset may be 
associated with a pain in the back, leading to a suspicion of variola 
or of meningitis ; the rash will soon differentiate the former, and the 
latter will soon be excluded by the subsidence of the pain and the 

1 This is the view now entertained of tabes dorsalis. 



vin DISEASES OF THE NERVOUS SYSTEM 293 

very rapid appearance of the paralysis; if meningitis were the trouble 
the pain would persist and the paralysis (if any) would be long 
delayed until the inflammation had had time to attack and destroy 
neuraxons. In adults, while the course of events is precisely the 
same, the general symptoms are much less pronounced, though the 
onset is equally rapid ; still, the age is in itself very important, for 
anterior poliomyelitis is as rare in adults as a mysterious, i.e. without 
obvious cause, neuritis is in children, and vice versa. On the other 
hand, peripheral neuritis rarely, if ever, has such an acute pyrexial onset 
with pain in the back ; it may have a smouldering fever lasting several 
days, or even a week or two (the febrile period in poliomyelitis is at 
most three or four days, generally only twenty-four or forty-eight 
hours), but then it has not the pain in the back ; if it has 
the pain in the back (lumbago and sciatica) it will not have the 
pyrexia unless this be associated with definite joint (rheumatism 
or gout) trouble. 

In those cases in which the acute poliomyelitis is only part of 
an acute transverse lesion, the early bladder and rectal disturbance 
and the complete paraplegic* anaesthesia will be sufficient to prevent 
mistakes. 

In the more chronic forms of trouble also the onset presents 
more striking differences than likenesses. Thus, in a peripheral 
motor lesion there is probably more wasting and paralysis in six 
weeks to two months than a case of progressive muscular atrophy 
will show in six months or a year ; and, again, the locality will be 
different, for in the neuritis the whole limb, or whole muscles, will 
have suffered (except in isolated nerve cases, which will probably 
have an obvious local cause), whereas in progressive muscular 
atrophy the changes will be confined to hand or foot (common 
type), or to shoulder muscles (upper arm type), spreading thence 
very slowly. The latter disease, progressive muscular atrophy, may 
be finally dismissed by stating that it has no other nervous features 
except a progressive weakness going hand in hand pari passu with 
the wasting, and R.D. is not to be obtained typically; while in 
peripheral neuritis the paralysis is out of all proportion in the 
early days to the wasting, and R.D. is typically present. The 
reason for these differences is obvious if we remember that in the 
system disease the cornual cells suffer one after another in very 
slow progression, and consequently individual neuraxons with their 
nutritional functions die and cause atrophy of individual muscle fibres 
or bundles ; while in the peripheral troubles many neuraxons are 
simultaneously involved. 



294 DIFFERENTIAL DIAGNOSIS 



B. — The Course of Established Symptoms 

The system lesions in their course, though sometimes appar- 
ently standing still, rarely or never lose their typical physical signs 
by which they have been diagnosed, but they frequently show im- 
provements or exacerbations quite unaccounted for by anything that 
can be called treatment or neglect. Peripheral lesions, on the other 
hand, proceed almost steadily in one of three directions : (i) straight 
downhill to the grave in less than a year or eighteen months; (2) 
downhill for so long as the cause acts and a little longer, and then 
with the cessation of the cause (usually alcohol) steady improvement 
sets in up to complete recovery, unless and until the cause again 
operates, when history repeats itself; (3) persist for an indefinite 
time without any apparent alteration. The perennial root of the 
tree is attacked in the system lesion ; in the other a branch is cut off 
which may or may not grow again, but, on the other hand, it may be so 
necessary to nutrition that the whole tree dies. 

We will now conclude the subject of cord and peripheral troubles 
with a few tables of special interest. 



Peripheral Neuritis and Tabes Dorsalis 
These often have the following in common : — 

1. Inco-ordination of movement ; 

2. Pains in limbs ; 

3. Absent knee jerks ; 

but more frequently they differ in the following : — 

Peripheral Neuritis. Tabes Dorsalis. 

Inco-ordination seldom a very Inco-ordination especially marked ; 
marked feature ; paralysis very paralysis and weakness for 

common. simple movements never 

present. 
Pain is in the nerve, never a girdle Pain shoots along a limb ; if a 
pain. girdle pain present it is very 

strong evidence (root symp- 
tom). 
Paresthesias common. Paresthesias rarely present 

Knee jerks sometimes exaggerated. Knee jerks never exaggerated. 
Viscera never affected. Visceral crises and disturbance of 

function common. 



DISEASES OF THE NERVOUS SYSTEM 



295 



Peripheral Neuritis. 
Eye affections may be present ; if so 
they are prominently complained 
of, and may stand as the sole 
symptoms ; optic neuritis or 
atrophy extremely rare. 



Tabes Dorsalis. 
Pupillary or oculo-motor troubles 
nearly constant, but in addition 
to other symptoms ; atrophy of 
optic nerve frequently found. 



Infantile Paralysis will resemble Diphtheritic Peripheral Neuritis 



(a) History of acute illness ; 

(b) Rapid onset of paralysis ; 

(c) Some wasting of muscles : 



but the two will probably differ in — 



Diphtheria. 

Acute illness almost certainly with 
prominent local (throat, vagina, 
wound, etc.) symptoms. 

Paralysis almost always of eye or 
palate first, and rarely of limbs 
at all. 

Wasting not great, and R.D. typi- 
cally present only in severe 
cases. 

Very symmetrical paralysis. 

May get worse for some days after 
onset ; recovery is always practi- 
cally complete if the patient does 
not die. 



Infantile Paralysis. 

Acute illness with only general 
symptoms or some pain in 
spine. 

Almost always of limbs only, very 
rarely cranial at all. 

Wasting considerable, and R.D. 
nearly constant, in some muscles 
at any rate. 

Ultimate paralysis characteristi- 
cally local and asymmetrical. 

After twenty-four or forty-eight 
hours any alteration is always 
in the direction of improve- 
ment ; recovery is never abso- 
lutely complete. 



Ataxic Paraplegia v. Peripheral Neuritis 



The combined motor and sensory phenomena may arouse 
suspicion of some peripheral affection, but the course of the cord 
disease is in itself almost sufficient to separate it from the latter ; 
the cord trouble is always slow in onset, and months elapse before it 
advances far, while the neuritis is almost invariably acute or sub- 
acute. The very marked inco-ordination, too, of the cord trouble, 
especially taken with the exaggerated knee jerk, adds further confirm- 
atory differentiation. 



296 DIFFERENTIAL DIAGNOSIS 



Amyotrophic Lateral Sclerosis v. Peripheral Neuritis 

Dr. Gowers says, " The wasting from disease of single nerves or 
at a plexus is sufficiently distinguished by its limitation, coupled 
with its rapid onset and associated sensory symptoms " ; and from 
some forms of multiple neuritis, he says, "It is necessary to wait 
for slower wasting in other parts than those first affected before a 
diagnosis can be made ; a careful search will generally reveal other 
symptoms of neuritis, and a known cause is usually obtrusive." 

Lateral Sclerosis v. Peripheral Neuritis 

Any affection of the pyramidal tracts can only be mistaken for a 
case of pure motor peripheral trouble. If sensory phenomena are 
present to an extent sufficient to attract attention the disease is not 
primary lateral sclerosis. The cases of motor neuritis which could 
rouse an idea of lateral sclerosis must be either of arms or legs. 
Now, if it be of the arms, the note at the bottom of p. 287 shows us 
that if the lateral columns are affected as high as the origin of the 
brachial plexus, the knee jerk is exaggerated and ankle clonus 
probably marked ; but, per co?itra, the peripheral brachial nerves have 
no such influence on the rest of the cord, and there will be no 
disturbance of reflexes lower down. The same test will also apply 
if the trouble be in the legs, for, except in the earliest stage of 
neuritis (and that arising in a manner and under circumstances 
which preclude all idea of lateral sclerosis), the knee jerk is absent 
and ankle clonus not to be obtained. 

Peripheral Neuritis v. Disseminated Sclerosis 

Insular sclerosis most usually offers a fairly typical symptom 
complex which cannot be mistaken for anything except functional 
(or hysterical) nervous disease ; but inasmuch as its very name 
implies a random distribution, it is possible that cases may arise in 
which the peripheral nerves are suspected. 

Of the many symptoms that may occur in disseminated sclerosis 
there are three which, notwithstanding its indiscriminate distribution, 
are almost constant, viz. — 

1. Intention tremors ; 

2. Nystagmus ; 

3. Increased knee jerk ; 

and it is as rare to find a case of peripheral neuritis exhibiting these 



DISEASES OF THE NERVOUS SYSTEM 



297 



three in combination without other obvious indications as it is to 
find a case of disseminated sclerosis in which they are not all three 
present. 

Disseminated Sclerosis v. Hysteria or Functional 
Troubles 

To distinguish the early stages of sclerosis from what is usually 
accepted as functional disease is probably to try and make a distinc- 
tion between identicals, for the death of neurons by sclerosis is in 
all probability preceded by a stage of functional debility in which 
recovery is certainly possible, but as the recognition and demon- 
stration of this recoverable condition is all-important from a thera- 
peutical and prognostic point of view, I have drawn up the following 
table of points most worthy of attention in rough order of im- 
portance. 



Functional. 

Tremors very common, but not 
so violent as to prevent comple- 
tion of intention. 

Nystagmus very rare and ill- 
marked ; double vision rare 
except very temporary. 

Knee jerks probably glib, but 
variable from time to time. 



4. Speech probably voluble, or 

obstinate silence; seldom 
scanning, varies from time to 
time. 

5. If bladder trouble at all it is 

retention, and pain not com- 
plained of. 

6. Optic neuritis or atrophy un- 

known. 

7. Recovery rather sudden and 

complete, and possibly no return ; 
if return it is sudden and in the 
same guise. 

8. Sensory hemi - anaesthesia not 

uncommon with recovery. 



Established Disseminated Sclerosis. 

1. Tremors so violent as frequently 

to quite frustrate intention. 

2. Nystagmus common and very 

distinct ; double vision not 
uncommon. 

3. Knee jerks grossly exaggerated 

and invariable ; should a 
patch have caught the reflex 
chain they will be absent, but 
still invariable. 

4. Speech scanning usually, and 

not variable. 



5. Bladder trouble frequent ; in- 

continence, stammering blad- 
der, and even painful retention. 

6. Optic atrophy if present is 

conclusive, for it is sclerosis. 

7. Apparent recovery curiously 

frequent, but return of symp- 
toms soon occurs ; may be in 
another guise. 

8. Hemi - anaesthesia rare, and 

what anaesthesia occurs is 
little likely ever to be removed. 



DIFFERENTIAL DIAGNOSIS chap. 

Functional. Established Disseminated Sclerosis. 

Perversion of will power a fre- 9. Perversion of will power not 

quent cause, or concomitant, often observed to any extent ; 

and very variable at times. if it is present it remains. 

Spasticity and inco-ordination 10. If spasticity or inco-ordina- 

variable from time to time. tion occurs it is likely to be 

permanent. 

If any wasting occurs it is 11. If wasting occurs it is likely 

likely to be general, and very to be local and fairly 

slow in onset, and arises from rapid, though when lateral 

mere disuse. columns are affected this 

will not hold. 



AFFECTIONS OF MEDULLA, PONS, AND 
CEREBELLAR PEDUNCLES 

In dealing with the peripheral nerves and spinal cord I have 
dealt at some little length with the points of differential diagnosis 
because the cases are more commonly met with, and because 
the problems of diagnosis are comparatively simple in themselves 
if due attention is paid to the elements that lead to conclusions. 

In dealing with intracranial troubles we are introduced at once 
to so much that is absolutely unknown, and still more that is only 
guessed at or in dispute, as regards anatomy and physiology, that 
complete diagnosis is frequently impossible, and I shall only 
attempt to sketch a clear outline of the principles of regional and 
pathological diagnosis, and introduce independently a few important 
subjects which are but ill remembered and worse understood by 
students. 

An accurate knowledge of the precise regional relations of the 
various tracts of fibres and groups of cells whose functions are more 
or less known is absolutely essential for a clear understanding of 
the diagnostic problems offered by disease in this region. The 
best way to learn this is by careful study of sections compared with 
the figures to be found in every text-book of anatomy. They may 
be tabulated for study thus : — 

Fibres of Pons, Medulla, and Cerebellar Peduncles 
A. — Old Tracts already noticed in the Cord 

I. Pyramidal, cross- Constitute the crossing of the pyramids, and then 
ed and direct ; the pyramidal tracts through the medulla, pons, 



DISEASES OF THE NERVOUS SYSTEM 



; 99 



functions purely 
motor. 



Antero-lateral 
ascending tract ; 
function to con- 
vey centripetal 
impulses. 
Direct cerebellar 
tract ; function 
centripetal (? en- 
tirely). 

Posterior col- 
umns : function 
centripetal. 
Bulk of unnamed 
white fibres of 
cord, function 
nearly or quite 
unknown unless 
commissural. 



and cerebral "crura." In tracing these down 
from the motor cortex it must be noted that 
some of them turn out to join the nuclei of 
origin of the motor cranial nerves, in which 
case the relationship between cortex and nucleus 
is always crossed, precisely the same as that of 
cortex and anterior cornua of cord. 

Some are traceable as fibres in the formatio 
reticularis, reaching thus the superior cere- 
bellar peduncles and so the cerebellar cortex ; 
others are lost in the formatio reticularis, and 
their further course unknown. 

Form a large part of the restiform bodies or 
inferior peduncles of cerebellum. This is the 
only known ending of these fibres. 

End in synapses with the cells of the funiculi 
gracilis, cuneatus, and rolandi. 

Constitute probably the bulk of the fibres of the 
formatio reticularis. Their destination is un- 
known and also their function, though they are 
assumed to unite successive segments of the 
mid-brain. 



B. — New Tracts of Fibres ; or in some cases New Names for Old Tracts 

Tract. Reaching to. 

{a) Function afferent, reach- 
ing the inferior peduncles 

.<2 of cerebellum as inter- 

U nal arcuate fibres, pass- 

3 ing to cerebellar cortex. 

v (b) Reach cortex of cerebrum 

o and cerebellum, or end 

'•§ in cells of formatio reti- 

S cularis (vide 5 above). 

<2 (c) Many go as arcuate fibres 

q to cerebellum, many also 
of unknown destination 

u ^ ■ and function. 



Originate in. 
I. (a) Cells of nuclei gracilis, 
cuneatus, and rolandi. 



(b) Unnamed white fibres 
of cord. 



(c) Olivary body and other 
cells in the region of 
the upper medulla. 

Direct cellebellar tract of 
cord, internal and external 
arcuate fibres. 



Cerebellar cortex and nuclei. 



O <-> 



3°° 



DIFFERENTIAL DIAGNOSIS 



Originate in. 

Cells of nuclei gracilis, 
cuneatus, and rolandi,also 
independent cells in for- 
matio reticularis, and 
many of cells of the 
olivary body. 

Begins by axons from cells 
of nuclei gracilis, cuneatus, 
and rolandi, added to by 
axons from cells of for- 
matio reticularis, of oli- 
vary body, etc. 

Cells of reticular formation 
at one end, cells near the 
nucleus of third nerve at 
the other, and from inter- 
mediate cells. 



6. From cortex of one cere- 
bellar hemisphere. 



Tract. 



o a 



c u ° 



Reaching to. 
Functions probably afferent, 
reaching cerebellar cortex 
by inferior peduncles. 



Is the principal afferent (? 
entirely) passage to brain 
from the cells in medulla, 
reaching to corpora quad- 
rigemina and optic thala- 
mus. 

Probably motor in function, 
serving for connections 
between motor cranial 
nerves, especially in their 
associated (quasi - reflex) 
movements, e.g. lips and 
tongue, the two eyes, etc. 

To the other hemisphere, 
probably engaged in co - 
ordination. 



Cells of the region 



Of funiculi — 
Gracilis, 
Cuneatus, 
Rolandi, 

In formatio — 
Reticularis. 



Cells of cranial 
nerves from three 
to twelve. 



I to 



Form some of the neuraxons of — 
) Fillet. 
{b) Internal arcuate fibres. 
) Others of unknown destination. 
Form neuraxons going to — 
(a) Reinforce fillet. 
(d) Connect different segments. 

(c) External arcuate fibres. 

(d) Reinforce posterior longitudinal bundle. 
Form the neuraxons of their respective nerves. 



Now, in applying these facts of anatomy and physiology to the 
problems of diagnosis, it cannot be too strongly insisted upon that 
in intracranial lesions, just as in peripheral (and cord) ones, there is 



vm DISEASES OF THE NERVOUS SYSTEM 301 

nothing essentially mysterious or beyond the power of the youngest 
student to grasp. The mystery, so far as there is any, lies simply 
and solely in our ignorance of the exact path of nerve impulses, 
and of the amount and nature of control and interference exercised 
by one neuron group over another. Lesions, of whatever nature, 
affect the structure and function of individual neurons in precisely 
the same way here as elsewhere, and this affection (whether of 
defect or excess) it is that constitutes our means of localising 
diagnosis. 

The elementary facts to grasp are : — 

1. That every anatomical nerve in the body has the power of 
communicating with, or of receiving messages from, the cortex of 
cerebrum and cerebellum for purposes of harmonious functioning in 
the healthy body. 

2. That for some reason (several explanations of the fact have 
been offered) that portion of the cerebral cortex which is thus in 
connection with a peripheral nerve is in the opposite named (right 
or left) hemisphere to that side in which occurs the peripheral dis- 
tribution of the nerve in question. 

3. That, per contra, the relationship of the cerebellar cortex to a 
nerve is an uncrossed one. 

4. That this crossing of impulses and of fibres lies — 

A. For motor nerves and impulses — 

{a) In the lower part of the medulla, so far as spinal 

nerves are in question. 
(b) For the cranial nerves, just a little nearer to the 

cortex than the nuclei of origin. 

B. For sensory nerves and impulses — 

(a) Distributed throughout the cord and medulla for 

the spinal ones, each nerve crossing at once. 

(b) For the cranial nerves, just a little nearer the 

cortex than the nuclei of origin. 

5. It is at once an obvious and necessary deduction from these 
elements of crossed influence that a lesion of a strand of fibres 
above, i.e. nearer the cortex cerebri than the nucleus of origin of the 
peripheral nerve in question, must exhibit its effects on the opposite 
side of the body to that on which the lesion lies. If it be at, or on 
the peripheral side of, the nucleus, its effects must be exhibited on 
the same side as that of the lesion : and further, from what has 



3 o2 DIFFERENTIAL DIAGNOSIS chap. 

been said on p. 252 about the function of the neuron cell, must 
almost inevitably be associated with some trophic alteration (excess 
or defect) in the muscles affected. 

6. A self-obvious statement, but one too frequently forgotten, 
that the closer the nerve fibres (or cells) lie together the more likely 
are they to be involved together by a small lesion. In this fact, 
however elementary it may seem, lies the clue to at least one-half 
of the localising problem. Thus, taking the motor side and a 
destructive lesion as an illustrative example, a cortical or sub- 
cortical small lesion may easily be understood to be capable of 
producing a monoplegia, but the nearer we get to the (anterior two- 
thirds of the posterior limb of the) internal capsule, the more fibres 
will be caught by the lesion, and the wider will be the peripheral 
area of disturbance, until when we arrive at the crura cerebri, pons, 
and medulla the motor fibres are collected so closely together that 
it is almost impossible but that a paralysis shall be at least a hemi- 
plegia, and possibly even a complete paralysis of all four limbs. 
Further, speaking of our present region — the mid-brain — it is almost 
impossible but that some at least of the motor cranial nerves shall 
have participated in the disturbance ; for this reason they give us 
tolerably exact information of the locality of the trouble. This 
will at once explain the following clinical experience, viz. that given 
a hemiplegia^ then if it is due to a lesion — 



In Crus Cepebpi. — The third nerve on the opposite side is nearly 
sure to be paralysed. Any other cranial paralysis will be on 
the same side as the paralysis of the body. 

In Upper Pons. — We may look for some weakness in the opposite 
fifth nerve (motor part), and possibly some anaesthesia, 
though there is a considerable distance between the motor 
pyramidal fibres and the sensory root of the fifth. 

In Lowep Pons. — Very probably a paralysis of the opposite 
seventh, because its peripheral course lies so close to the 
motor fibres which are destroyed. (The explanation of the 
contraction of the pupils, a constant feature, is not quite so 
obvious.) 

In Medulla. — We may look out for a paralysis of the opposite 
sixth, very possibly of the opposite seventh, because the 
seventh nerve winds round the sixth nucleus. (A paralysis 
of both sixth nerves is not such a precise indication, owing 



DISEASES OF THE NERVOUS SYSTEM 303 

to their exposure to pressure between the pons and the 
bone.) In the lower part of the medulla one twelfth nerve 
or a spinal accessory is very likely to be affected, leading to 
deviation of protruded tongue, or to paralysis of a vocal 
cord. 



CRANIAL NERVES 

The last paragraph has shown the importance of these nerves as 
indicators of locality of a lesion. I propose now to add a few notes 
on the individual nerves and their lesions. 

First, or Olfactory. — This, strictly speaking, is not a nerve but an 
integral part of the cerebral cortex. Clinically, if the sense of smell 
is impaired, we must first suspect and investigate the external 
cavities. If these are declared free from suspicion the trouble may 
be situated in the anterior fossa of the skull, causing pressure on 
the olfactory bulbs. The cortical connections of the bulbs are 
supposed to exist in the tip of the temporo-sphenoidal lobe, so that 
in cases of suspected abscess or tumour, interference with the 
faculty of smell is a suggestion that the lesion is not far from that 
situation. 

Second, or Optic. — Like the olfactory, is a distinct outgrowth of 
the brain, with a primary connection with the corpora quadrige- 
mina. Its cortical representation is found (a) in the occipital lobes 
for coarse optical impressions, i.e. for an appreciation of the fact 
that something is affecting the optic nerves ; (b) in the supra- 
marginal and angular gyri round the end of the sylvian fissure for 
optical perceptions and judgments, i.e. for an appreciation of the 
precise object that is stimulating the optic nerves, and its exact 
nature and associations. Hence, as regards localising deductions 
from the nerve, we have — 

(a) Optic neuritis (vide p. 324). 

(b) If hemianopia be due to a lesion of the optic tracts the 

pupil will not react when light is thrown on the blind 
half of the retina, because the lesion is in front of the 
centre for reflex of light ; if it lies between the corpora 
quadrigemina and the optic lobes the pupil will react, 
but the patient will not perceive that anything is stimu- 
lating the retina ; if the lesion is between the occipital 
and the supramarginal lobes he will perceive the object, 



3 o4 DIFFERENTIAL DIAGNOSIS chap. 

but will not judge its nature correctly. (This is the 
condition known as word blindness when testing a case 
of aphasia.) 

Third, Fourth, and Sixth. — These nerves, taken collectively, 
form the motor apparatus (with muscles) of the eye-balls, built and 
arranged to subserve the purpose of single vision with two eyes, for 
which very accurate associated action of the muscles is required. 
This is provided for undoubtedly by the close approximation of the 
nuclei of the nerves, and by the posterior longitudinal bundle 
serving as a rapid means of communication ; hence it certainly 
follows that nuclear lesions of these nerves or of the posterior 
longitudinal bundle will cause squinting, or at least double vision 
(squint is merely a deviation of the visual axes from their normal 
position visible to the observer). Such lesions are known, though 
not very common ; their exact discussion would be too intricate to 
follow out here. It must not be forgotten that these three nerves 
lie very close to one another and to the orbital branch of the fifth 
at the entrance to the orbit, so that a tumour or sclerosing lesion in 
that situation may produce a total paralysis of all four nerves. 

Simpler problems are presented by considering the individual 
nerves and their branches, i.e. peripheral lesions. 

Third Nerve. — If affected by a crural lesion it is probable that 
there will be a complete paralysis of the whole of the third on the 
opposite side to that on which the paralysis of the body is said to 
be. If affected in the more peripheral parts of its course, it is more 
probable that the paralysis will be incomplete, i.e. of one or more 
branches only. The reason for this is better discussed along with 
pathological diagnosis. 

Fourth. — To this nerve the same remarks apply as to the third, 
remembering that it only supplies one muscle, viz. the superior 
oblique, which assists in dowfizvard movements of the globe. Hence 
double vision on looking downwards only. 

Fifth. — When affected at or above its nucleus never, according 
to Bastian, exhibits trophic, vasomotor, or secretory disturbances of 
function ; when affected in its peripheral course does exhibit such 
disturbances in the appropriate area of distribution. 

Sixth. — As above remarked, the exposed position of these nerves 
between the pons behind and the bone in front deprives a double 
paralysis of much localising value, but if one only is affected we have 
strong ground, in an otherwise doubtful case, for believing that the 



viii DISEASES OF THE NERVOUS SYSTEM 305 

lesion is in the medulla or in front of the pons ; in front, that is, as 
regards the cranial fossae. If one sixth and the same named (right 
or left) seventh are involved together, we can fix the lesion pretty 
accurately as at that spot in the medulla where the seventh nerve 
winds round the sixth nucleus. 

Seventh. — In small lesions at or above, i.e. nearer the cortex, its 
nucleus, it is a clinical fact that the occipito-frontalis muscle almost 
invariably escapes, probably because the muscle is most commonly 
used reflexly, and stimuli reach it by the posterior longitudinal 
bundle. If the nerve is affected between the brain and the bottom 
of the internal auditory meatus it is very likely that deafness of the 
same ear may be found, because the seventh nerve lies in actual 
contact with the eighth. In lesions beyond this point, up to the 
exit from the stylomastoid foramen, it is likely that the paralysis will 
be absolutely complete. Beyond this point individual branches 
may be caught by a lesion, but we shall have probably gross mani- 
festations of a swelling (parotitis, etc.) or inflammation to help us 
outside the skull. It is also to be noted that in peripheral lesions 
there will be no associated hemiplegia. 

Eighth. — In central lesions it is not likely that the auditory 
nerve will suffer alone, its nuclei are too wide spread. In peripheral 
lesions it will be likely to suffer alone, or, as above noted, in con- 
junction with the seventh only of the same side. 

Ninth, Tenth, and Eleventh. — Individual lesions of any of these 
nerves alone at their nuclei are excessively rare. A central lesion 
of any of them will, therefore, locate itself in the medulla by being 
associated with an affection of all three. A peripheral lesion will 
define itself by features external to the skull. 

Twelfth. — The tongue is so intimately connected with the power 
of articulate speech as to lead to a conclusion that the cortical 
representation of the twelfth nerve is to be found in Broca's con- 
volution on the left side, and in a corresponding area on the right 
hemisphere ; and we find that a lesion on the left side (? on the 
right side in left-handed people) in Broca's convolution, or between 
it and the twelfth nuclei, disarranges the function of the tongue so 
far as that subserves speech (pure motor aphasia). 

Again, in deglutition, and in practically all uses of the tongue, 
the two halves are so accustomed to work together that it would 
seem a great convenience (or, probably, almost a necessity) that 
they should be capable of being stimulated from either side of the 



3 o6 DIFFERENTIAL DIAGNOSIS chap. 

brain. Furthermore, as a matter of anatomical fact, the nuclei of 
the right and left twelfth nerves lie so close together in the floor of 
the lower half of the fourth ventricle as to be almost intermixed. 
Hence, as a matter of clinical experience, we find that (barring 
speech defects) in lesions above the nuclei, if a one-sided paralysis 
of the tongue occurs, it is likely to be incomplete and also to 
be comparatively temporary, and certainly unassociated with any 
trophic lesions. In lesions at the nuclei the paralysis is almost 
sure to be bilateral, and (vide p. 252) associated with atrophy. 
From lesions peripheral to the nucleus we may again get a one- 
sided paralysis, but this time with trophic lesions. 



DISEASES OF THE BRAIN 

What we know about the brain is, that it is composed of neurons 
and supporting (mechanical and nutritional) tissue. The former 
so arranged and connected as to subserve in the best possible 
manner the great purpose of bringing us into more or less har- 
monious communication with the world at large — co-ordination of 
functions in the very widest meaning of the word. Here resides 
the consciousness of change in the environment, both internal, of 
organs, and external, of the body, and here is initiated the necessary 
process to adapt everything to that change. 

What we hypothecate is, that through these neurons, and their 
synapses with one another, messages can with very great ease 
pass from one hemisphere to the other (commissural fibres), 
or from every part to every part of the hemisphere of the same 
side (internuncial fibres), and also with both direct and 
crossed influence from cerebral to cerebellar cortex and me- 
chanisms. 

To completely analyse the tracks by which this is done — even 
those which are tolerably well known — would require a large volume, 
and would in the present work serve no useful purpose. So far as 
bedside diagnosis is concerned, the principal difficulties in the way 
of accuracy are : ( 1 ) want of precise knowledge of actual structural 
continuity of tract with tract; (2) a still greater lack of precision in 
knowledge of functional continuity; (3) the fact that direct patho- 
logical lesions, and still less their effects as regards pressure, so 
very seldom confine themselves to those individual tracts, or tracks, 
about which we think we know something. 



DISEASES OF THE NERVOUS SYSTEM 



3°7 



Frontal. 



The following tables give some of the principal points of localisa- 
tion, either approximately proved or strongly suggested : — 

Cortex of the Brain — 

Ascending parietal, as- Possess the function of initiating the motor 
cending frontal, and side of movements in various parts of the 

corresponding body on the opposite side. In this area 

median cortex. of cortex are represented in order from 

above downwards the foot, leg, arm, 
face, so that a pure cortical destructive 
lesion produces weakening of these move- 
ments. For irritative lesions, vide Jack- 
sonian Epilepsy, p. 309. 

Suggestively the seat of connected thought 
and reasoning ; lesions here have, in some 
cases at least, impaired this power, e.g. 
general paralysis of the insane. In- 
dubitably this region comes into structural 
continuity with the anterior limb of the 
internal capsule, and so functionally is 
supposed to be connected with the cere- 
bellar and occipital cortex. 

Probably in the main the seat of subjective 
consciousness of sensory stimuli ; it is 
almost certainly proved also to be the 
seat of the primary registration of optic 
impressions. 

Proved almost conclusively to be the seat of 
the final registration of optic impressions, 
i.e. visual concepts as opposed to mere 
percepts, and to be for this purpose in 
close connection with speech (on its 
motor side) and appropriate common 
motor areas. These facts are such, at 
least, for the left hemisphere {vide Optic 
Nerve). 

Stands in precisely the same relation to 
auditory stimuli that the supramarginal 
does to visual ones {vide Auditory). 

Represents the olfactory sense in a similar 
though perhaps less efficient manner. 

Very few or no facts essentially proving a 
local or definite function. 
Cere- All we can say about this is, that when, 
by damage to its peduncles, messages 



Occipital. 



Supramarginal and an- 
gular. 



Superior temporo- 
sphenoidal. 

Tip of the temporo- 

sphenoidal lobe. 
The rest of the cortex. 



Cortex of 
bellum. 



3oS DIFFERENTIAL DIAGNOSIS chap. 

are unable to reach the cortex, defects 
of equilibration become a marked feature 
in the disease, but we cannot say more 
precisely how or why these are caused. 

White Matter underlying Cortex — 

Inasmuch as this is engaged in carrying messages to and from 
the cortex, it is difficult, or even in many cases impossible, to 
differentiate lesions of it from those of the overlying gray matter. 
All that can be said, in general terms, is, that the nearer to the 
cortex the more likely is subjective consciousness — apart from a 
mere unconsciousness in the ordinary sense of the word — to be 
implicated in the pathological disturbance, and on the motor side 
the less likely are we to get mere twitching (or loss of power) in 
groups of muscles as opposed to actual purposive (but unconscious) 
movements or weakening of such movements. We know a little 
about some tracks, or tracts, in the white matter. Thus : — 

That in the frontal lobes is collected mainly into the anterior 
limb of the internal capsule. We do not know much about lesions 
of this, except that we should expect inco-ordination of movement 
to some extent, and incoherence of thought, i.e. we only know it so 
far as we know the function of the frontal cortex. 

That corresponding to the motor cortex is gathered together as 
the corona radiata, and then more concentrated still in the anterior 
two-thirds of the posterior limb of the internal capsule. As it 
conveys the motor impulses lesions of it will cause hemiplegia or 
hemiconvulsions. 

That corresponding to the occipital cortex conveys impressions 
to the sensorium from everywhere, per the posterior third of 
the posterior limb of the internal capsule, and lesions should 
produce hemiansesthesia and lesions of sight corresponding to what 
has already been said on that subject : also interference with the 
afferent impulses necessary for co-ordination. 

That of corpus callosum can only be said to connect the two 
hemispheres ; of its special function, and of evidence of its lesions, 
we can say nothing here. 

Basal Ganglia with their Fieres and Cells — 

Of the corpus striatum, optic thalamus, and cells of the teg- 
mentum of the crura cerebri, it is impossible to say anything 
definite without going into minute detail. We recognise in them 
anatomically complete neuron groups (cells and processes) in very 



vin DISEASES OF THE NERVOUS SYSTEM J 309 

intimate connection with one another and with cortical groups 
— evidently very complex and delicate mechanisms for the rapid 
distribution and adjustment of nerve stimuli ; but, notwithstanding 
the attention they have received of late, we are still almost as much 
in the dark now as ever we were as to the precise part played by 
them in conscious, or in reflex life. We can still only say that the 
corpus striatum probably has something to say to the correct adap- 
tation of means to ends on the motor side, while the optic thalamus 
and tegmentum play a similar role in connection with the correct 
appreciation of afferent stimuli on their way to the cortex. Of the 
corpora quadrigemina and gray matter in connection with them we 
can say that they play a conspicuous part in the correct manipulation 
of the eyes, including in that term not only gross movements but 
also accommodation and reflex to light. 

We may now conclude this elementary outline of localisation of 
the brain functions by a note on one or two points of special diag- 
nostic interest as illustrations. 

ON THE MOTOR SIDE 

A. — Jacksonian Epilepsy — 

This term has been given — in honour of the first accurate investi- 
gator of the phenomena — to attacks of convulsive movements which 
commence locally in an extremity, or in the face, and are due to an 
irritant lesion of some kind in that portion of the rolandic (or motor) 
area corresponding to the given peripheral commencement of the 
movements. Any given attack may be quite local, and limited in 
distribution almost to the spot originally attacked, or it may be 
spread more and more widely so as to involve the other limbs 
of the same side, and even those of the other half of the body, and 
may even end in unconsciousness, hence it may closely resemble 
idiopathic epilepsy. The important points to remember about it 
are, that for the same patient — 

(a) It invariably begins in the same place (thumb, great toe, and 

mouth are the commonest). 

(b) It invariably spreads in the same direction, though not 

necessarily to the same extent; the extent apparently 
depends upon the nature and amount of the temporary 
exciting cause of extra activity, but the direction is prob- 
ably governed by lines of least resistance, which soon 
become established in any patient, and remain constant for 
that patient. 



310 DIFFERENTIAL DIAGNOSIS chap. 

(c) It is always followed by an (at least temporary) paralysis of 

the convulsed muscles which — 

(d) Is always most marked in the muscles first affected. 

Thus its presence is a very strong piece of localising evidence 
for an irritant in a particular part of the rolandic region. In the 
above particulars it may closely resemble idiopathic epilepsy, especi- 
ally if the aura of the latter is local, but the following points will 
usually serve to distinguish them : — 

Jacksonian. Idiopathic. 

i. Inmost cases either a marked If cause be present it will be in the 

and obvious cause, e.g. shape of a family history or some- 

traumatism, or evidence thing general, not local. Ab- 

suggestive of a neoplasm as sence of evidence of gross intra- 

cause. cranial disease other than that 
afforded by the fit. 

2. The commencement always Onset not often local in the situa- 

local, and movement pre- tions chosen by Jacksonian ; when 

cedes sensation. it is thus local sensation precedes 

movement. 

3. No tonic stage, at least not Tonic stage nearly constantly pre- 

marked. sent. 

4. Comparatively rarely goes so Loss of consciousness is a constant 

far as general loss of con- feature, though it may be only 

sciousness. momentary. 

5. After a fit, paralysis, or at Paralysis after a fit not present, a 

least weakness, is a marked feeling of tiredness in general the 

feature in the locality of the only evidence of motor distress, 

commencement. 

6. No sleepiness after a fit. Sleepiness very frequent after a fit. 

B. — Other Motor Disturbances of Voluntary Move- 
ments — 

Besides Jacksonian epilepsy, the following involuntary movements 
are usually assumed to be due to damage of the brain, because (1) 
they are usually associated with mental deterioration ; (2) they 
cease during sleep as a rule ; (3) they are more complex in gross 
aspect than we are accustomed to see in pure spinal movements. 

Paralysis agitans. Coarse rhythmical movements, usually of the head 

and hands, more marked during inaction ; 
often, too, these are of the hemi- type, another 
argument for a brain origin. 



viii DISEASES OF THE NERVOUS SYSTEM 311 

Chorea. Coarse, involuntary imitations of purposive move- 

ments, continuous during waking hours ; also 
often of hemi- type. 

General paralysis of Principally of lips and tongue during speech, also 
insane. seen in the limbs ; the morbid anatomy of 

this disease is known to be a fine cortical 
sclerosis. 

Chronic alcoholism Coarse tremor of hands upon attempted fine 
or mercurialism. movements. 

Athetosis. Peculiar rolling movement of affected digits ; 

frequently post-hemiplegic, and then indicates 
that the lesion is probably near the cortex. 

C. — Symmetrically used Muscles — 

In those symmetrical muscles of the two sides of the trunk and 
face which are almost never used independently in health, e.g. inter- 
costals, eye muscles, etc., complete paralysis is never seen from a 
one-sided central lesion ; the explanation of this, known as Broad- 
bent's hypothesis, is that such muscles are stimulated into action 
with nearly equal facility from either hemisphere, either through the 
corpus callosum or through mechanisms in the mid-brain (? cere- 
bellum). 

ON THE SENSORY SIDE 

Information and facts are much less definite and numerous in 
considering afferent than efferent impulses. When once the sensory 
impulse has reached the medulla on its centripetal journey we know 
little or nothing about it and its neuron complexes, or series of 
complexes, till it reaches the posterior third of the posterior limb of 
the internal capsule. It is clinical observation that has taught us 
that afferent impulses are absolutely necessary for the co-ordinate 
and harmonious working of the whole body ; but, so far as inco- 
ordination in the narrower sense of mere movement is concerned, 
we have only one fact of importance to guide us, viz. that if inco- 
ordination be due to spinal or peripheral lesions, as in tabes, in all 
probability the knee jerk will be absent, if it be due to intracranial 
lesions the knee jerk will be either natural or exaggerated. 

Hemianesthesia — 

Due to an organic cause is an excessively rare phenomenon 
when standing alone ; when with hemiplegia it almost conclusively 
proves a lesion of the internal capsule, because it is only here that 



i 



312 DIFFERENTIAL DIAGNOSIS chap. 

the sensory fibres are sufficiently close together and to the motor 
ones to be thus affected by a lesion small enough to not cause such 
an interference as will either rapidly prove fatal or have such an 
effect upon consciousness as to prevent trustworthy observations. 

N.B. — This last statement should be carefully borne in mind, for 
it is the clue to the reason why many bizarre effects in cerebral 
troubles have not been noted ; if the lesion is great enough to 
damage tracts widely separated, it is either multiple or so large as to 
cause rapid death. 

Hemianaesthesia as the sole evidence of disease is almost in- 
variably due to functional and recoverable causes probably affecting 
the internal capsule. 



ON THE MENTAL SIDE 

If there be no pyrexia or other evidence of local disease outside 
the nervous system, then, qua localisation from mental phenomena, 
all we can say is that the disease is above the pons and crura, and 
in all probability is in the cortex of the cerebrum. They arise in 
all probability from a loosening of, or at least alteration in, the 
synapsial connections of the cortical neurons. Clinical experience 
would tend to suggest that the frontal lobes have more to do with 
the mind than any other part, but nothing beyond this can be said. 
****** 

We have now to deal with the differentiating points, and especially 
to note them as regards the intracranial portion of the system. 

I propose to discuss the matter, so far as necessary, under the 
following headings : — 

i. Traumatism. 

2. Functional troubles. 

3. Ordinary organic lesions. 

1. Traumatism 

Speaking generally, the incidence of an accident of gross nature 
and its immediate results are easy enough to appreciate, but there 
are a few cases of nerve troubles not perhaps usually included in 
the term, but which, I think, should be so included, for they are 
essentially traumatic in constitution. Chorea after fright, neuritis 
or so-called occupation neurosis, i.e. after prolonged special use of 
nerves, and the results of shock, are illustrations of my meaning. 



viii DISEASES OF THE NERVOUS SYSTEM 313 

Probably in all there may be an underlying functional or structural 
weakness of the nervous system, but this does not really affect my 
point. 

If we thus widen our conception of traumatism, we have the 
following separate groups of possible results : — 

(a) Gross laceration or bruising of tissue, with acute inflamma- 
tion, followed or not by suppuration and abscess forma- 
tion, of all of which the traumatism, with entry of pyogenic 
germs, is at once an obvious, complete, and satisfactory 
diagnostic explanation. 

(&) Tumour of malignant or simple character, where again 
nothing more need be said, for the tumour is either a 
blood clot, or it remains in the shape of a cyst, or is of 
a heteroplastic nature — there are too many cases on 
record of the last incident to leave any room for discus- 
sion as to the sequence of events. (For further notes, 
vide -p. 323.) 

(c) Sickness or degeneration of neuron processes, which may 
end in recovery, or in ultimate death and sclerosis of the 
whole neuron, according to the severity of the changes 
started in it and the general recuperative power of the 
animal functions of the whole body. 

This is, I think, the explanation of such cases as those mentioned 
above — shock, chorea, occupation neurosis — and possibly others. 
I believe that the potential (to use an electric analogy) of the 
stimuli sent through the neuron processes has been so high, or the 
current so long continued, as to have heated, melted, or disturbed 
the molecular constitution of the wires or connections, with resultant 
temporary or permanent loss of conducting power. This analogy 
must not be driven too close in detail, but in broad outline seems 
to me to offer the best explanation of such cases. However this 
may be, the relationship of external cause with the clinical symptoms 
is admitted by all. Of the diagnosis of chorea and shock little 
needs to be said; their features are unmistakeable. The only 
problem connected with them is whether the connections or wires 
of the nerve mechanisms can be repaired, and this point can only 
be proved by time. Suffice it to say, that repair is the rule, though 
this may be not quite complete. Of the identification of an occu- 
pation neurosis or neuritis one can only emphasise the great fact, 
from which, indeed, they derive their name, viz. that the pain or 
spasm, or inco-ordination, complained of by the patient is only pro- 



3 i4 DIFFERENTIAL DIAGNOSIS chap. 

duced by the special movements peculiar to the particular occupa- 
tion (writing, violin playing, etc.). None of them appear when the 
same nerves and muscles are used for other combinations. This is 
at least true in the early stages of the malady, but recent observa- 
tions tend to show that a definite neuritis does frequently exist. If 
and when this is so, it is easily explained on the above hypothesis. 
The fact that these neuroses are exhibited only in the performance 
of one special combination of movements is a strong argument in 
favour of a primary lesion in the cortex, where combined movements 
and not muscles are chiefly represented {vide supra, p. 257). It may 
also be mentioned that the following, amongst others, suggest a 
cortical seat for the troubles causing chorea and shock : — 

(a) That they are practically always associated with some altera- 

tion in the mental or psychological conditions of the 
patient. 

(b) That they very frequently exhibit themselves on one side of 

the body only. 

(c) That the trouble is exhibited by complex combined move- 

ments which are originated in the cortex. 

2. Functional Troubles 

On p. 275 will be found a definition of the term "functional," 
and the tables and remarks throughout this section may be used to 
locate the weakened neurons, for it is only by perverted function 
as exhibited peripherally that we can locate the weakness. Here I 
wish to draw attention to a division of these cases into (a) those 
due to traumatism as defined above, and (p) those due to a general 
constitutional cause resulting in a loss or perversion of will power. 
In the latter group of cases, constituting the hysteria of the layman, 
or the "cussedness of the individual," I believe that the primary 
and essential lesion resides in the cortex of the brain (? and cere- 
bellum), and consists in imperfections of the synapses of the inter- 
nuncial neurons with one another, perhaps associated with altered 
stability of the molecular constitution of the neurons themselves. 

3. Ordinary Organic Lesions 

There is one exceedingly important general observation to be 
made which links all these into one. It is this : We must never for- 
get the great frequency with which acute vascular lesions are found 
as a complication — very frequently forming the closing episode — in 



vin DISEASES OF THE NERVOUS SYSTEM 315 

the more chronic troubles, particularly in tumours and in sclerosing 
lesions ; so that, while recognising the acute condition, we must 
never omit to inquire very carefully for evidence of a possible pre- 
existing chronic trouble {vide also pp. 272 and 278). By putting the 
definite question, " When was the patient last quite well and in his 
normal condition ? " and further, by inquiring for any slighter mani- 
festations of ill-health that may have preceded the actual attack 
for which our assistance is required, we shall not only get evidence 
of a second lesion if one exists, but we shall also gain informa- 
tion that may be of the greatest service in deciding between the 
various possible causes of the attack. 

We may now proceed to an analysis of the lesions themselves 
individually. Those which I propose to discuss briefly are : — 

Inflammation, haemorrhage, thrombosis, and embolism (acute 

vascular lesions). 
Idiopathic affections of neurons. 
Tumours. 

The following analysis, with the appropriate change in locality, 
will frequently apply as well to the cord and nerves as to the brain. 

Broadly speaking, they divide themselves clinically into two 
groups: (1) irritative, (2) destructive lesions; but the distinction, 
though useful, cannot be maintained in its entirety. For in the 
life history of an irritative pathological lesion (physiological stimuli 
apparently have no such limits) there is to be noted, first, a period 
of excessive functioning in the affected neurons (pain, paraesthesiae, 
twitchings or contractions of muscles), followed by a period in 
which this excess becomes less and less, until it becomes a nega- 
tive quantity, finally function is completely abolished (anaesthesia 
and paralysis), in which stage the symptoms are those of a para- 
lysing lesion — another reason for carefully ascertaining the whole 
history of the case. Then, again, the distinction of irritation v. 
destruction will depend in some cases on the situation of the lesion, 
meninges, or perineurium v. bulk of brain, cord or nerve strands. 
Inflammation, haemorrhage, and frequently also tumour, will at all 
times offer good examples of this variability with locality. 

Acute Vascular Lesions 
Acute Inflammation. 
(For diagnosis of Peripheral Neuritis, vide pp. 281 et sea. 
and pp. 292 et sea.) 

As it attacks the central nervous system it occurs in two well- 



316 DIFFERENTIAL DIAGNOSIS chap. 

marked forms, i.e. meningitis and encephalitis or myelitis, which 
require separate notice. 

Of the Membranes, Meningitis. — Here, as anywhere else, acute 
inflammation excites general symptoms, viz. pyrexia, with malaise 
and discomfort. The special points leading us to locate it in the 
nervous system are the concentration of the pain in the back, or 
in the head, with rapid onset of grave symptoms of implication of 
nerve matter, or of pressure on it (affections of cranial nerves — 
squint, facial paralysis, etc. — vomiting, optic neuritis, unconscious- 
ness, jumping of muscles, feebleness of gait, or paraplegia, etc.). In 
its irritative stage it may require separation from meningeal haemor- 
rhage or tumour. From the former, its slower onset and the pyrexia 
will be sufficient ; from the latter, the pyrexia again and its more 
rapid (a day or two at most v. a week or two at least) onset 
should usually leave no doubt. 

In its paralytic stages it becomes essentially a cortical myelitis 
or cerebritis, and only the history shows that such began as a 
meningitis. 

Of the Cord. — The rapid onset of a complete paraplegia could 
only arouse suspicion of blocking or rupture of a vessel apart from 
a myelitis. Thrombosis or plugging of spinal vessels is so rare as 
to be a mere curiosity, but both this and haemorrhage will be in 
their earlier stages sufficiently separated from myelitis by their 
absolutely sudden onset, and by the absence of pyrexia. In their 
later stages all three lesions would be identical. 

Of the Brain. — A primary cortical acute cerebritis is extra- 
ordinarily rare. If it occurred it would precisely resemble an acute 
meningitis, except that there would be a more rapid onset of para- 
lytic phenomena, especially in the limbs (vertical meningitis), or in 
cranial nerves (basal meningitis). 

Acute primary medullary cerebritis, i.e. in the mass of the 
brain, is practically only known in the shape of an abscess, and 
then the principal point is to separate it from a tumour. Their 
likenesses and differences may be summed up thus. Both will be 
equally likely to have — 

i. Vomiting. 

2. Optic neuritis. 

3. Headache (intense). 

4. Localising paralytic phenomena, or irritative. 



vin DISEASES OF THE NERVOUS SYSTEM 317 

On the other hand, they will probably differ as follows : — 



Abscess. 

A history of some peripheral 
suppuration — ear, nose, and 
other discharges — which has 
possibly ceased just previous 
to symptoms of cerebral 
trouble. 

Symptoms may quite possibly 
come on with great rapidity, 
and rapidly get more serious. 

Temperature a little raised, or 
more probably subnormal. 

Irritative phenomena rare, para- 
lytic phenomena at once or 
rapidly coming on. 



Tumour of other Nature. 
Probably no such history, but there 
may be a tumour elsewhere sug- 
gestive of a primary growth, to 
which the cerebral one may be 
secondary. 

Symptoms rarely increase with 
great rapidity unless it be with 
instantaneous exacerbation, indi- 
cating haemorrhage into tumour. 

Temperature either quite normal, 
or with greater and more irregu- 
lar ranges than in abscess. 

Irritative phenomena commoner, 
and lasting longer than in ab- 
scess. 



Hemorrhage, Thrombosis, and Embolism — 

The one essential feature common to all these, and the one by 
which they are as a group separated from all other lesions, is the 
instantaneous rapidity with which their symptoms commence, and 
speedily reach an acme. The two latter never as a simple diagnos- 
able lesion occur in the meninges, but the former frequently does 
so, and it is of some importance to distinguish this situation of it 
if we can : — 



Meningeal Haemorrhage. 

1. Commoner when idiopathic in 

young subjects. 

2. Very rare, except as the result 

of traumatism, forceps at birth, 
e.g., or blows on the head or 
back. 

3. Commencement of symptoms 

sudden, but generally some 
minutes or even hours before 
they reach their acme, i.e. 
more ingravescent. 



Haemorrhage into Bulk of Brain or 
Cord. 

Commoner in older subjects when 
without exciting cause. 

Very' common, without any history 
of traumatism : is equally rare 
as the result of violence, unless 
this be very severe. 

Instantaneous commencement, and 
acme reached almost with the 
same rapidity ; gradual ingra- 
vescence is much rarer, though 
well recognised as occasionally 
occurring. 



318 DIFFERENTIAL DIAGNOSIS chap. 

In this point of contrast it is obvious that exceptions must 
occur in connection with the size of the vessel which has ruptured, 
e.g. the middle meningeal or the basilar, on the one hand, the 
symptoms of which will be indistinguishable almost from intra- 
cerebral haemorrhage ; or, on the other hand, a very small branch 
of an intracerebral artery, the symptoms of which may be very 
slowly ingravescent. Concussion, or brain bruising, is another 
exception, but its onset is always traumatic and sudden. 

„ r . . TT , Haemorrhage into Bulk of Brain or 

Meningeal Haemorrhage. s c , 

4. The symptoms usually go The symptoms cannot be said to 

through an irritative stage, have any irritative stage ; they 

which is easily observable are destructive from the earliest 

and may be prolonged (pain time of observation, 
or convulsive movements). 

5. The subsequent course may Recovery never complete, and the 

show complete recovery, focal lesion will always be found 
though possibly an irritative to be a destructive one. 
focus may be left behind. 

In discussing the separation of the three troubles as they occur 
in the bulk of the brain or cord, it must be admitted once for all 
that a positively certain diagnosis (ante-mortem) is impossible, but 
a more or less intelligent and probably correct guess may be 
hazarded by attention to the following points : — 

1. That in the spinal cord the communication of the vessels is 
so free and easy that embolism and thrombosis are of the very 
rarest occurrence of sufficient extent to cause a definite paraplegia. 

2. Age. — Though the cause leading to embolus direct from the 
heart (acute endocarditis) is commoner in young subjects, and also 
syphilis and tubercle as active causes of local thrombosis, yet none 
of them cease absolutely as age advances. Moreover, atheroma, 
another principal cause of thrombosis or embolism (from debris), is 
distinctly an affection of advancing years. Hence age, per se, gives 
us no very strong and leading guidance ; nevertheless it must be 
stated that, ceteris paribus (which they seldom are), the older the 
patient the more do our thoughts go in the direction of haemorrhage. 

3. Marked premonitory symptoms of slight attacks are likely to 
make us think of thrombosis, especially if syphilis is present, or 
tubercle a probability. The reason for this is that preliminary 
small haemorrhages are rare, and so also, I believe, are small 



viii DISEASES OF THE NERVOUS SYSTEM 319 

emboli, while as an artery gets gradually obliterated we should 
expect premonitory evidences of disturbed nutrition in areas which 
are ultimately going to die. 

4. State of Consciousness. — If we bear in mind that haemorrhage 
forces asunder (by a pressure increasing as the cube of the radius 
of its bulk) the fibres of the brain, and adds materially to the bulk 
of the intracranial contents by blood which should be escaping by 
the veins, thus increasing the intracranial pressure ; if, too, we 
bear in mind that loss of consciousness (under the circumstances 
we are now considering) is probably due to increase of pressure on 
the cerebral cortex, or to violent impressions upon it, and then 
consider that the plugging of a vessel from any cause has no such 
tendency, we shall see the probable explanation of Trousseau's 
statement (which is, I believe, still in accord with clinical experi- 
ence), that " Whenever hemiplegia, complete and absolute " (there- 
fore due to a rather serious lesion), " occurs suddenly " (therefore 
due to vascular lesion) " without the loss of consciousness " (there- 
fore without much pressure), "it is more likely to be due to 
softening (plugging) than to haemorrhage. " 

5. State of Heart. — If in a young subject, otherwise in usual 
health, we hear cardiac bruits, they will be, ipso facto, suggestive of 
embolus, provided the heart is acting fairly quietly and regularly, 
and the more suggestive the more recently the bruits are known to 
have developed. If, on the other hand, we find a powerful heart 
acting violently with or without bruits, we suspect that this power 
has ruptured a weakened vessel, especially if the attack (hemiplegia) 
came on during exertion or excitement (one of the great dangers of 
alcohol when taken by a person with damaged vessels). Finally, 
if the heart beat is very feeble, as after a severe illness of any sort, 
and during convalescence, the feebleness of the circulation is sug- 
gestive of thrombosis, either locally at a distance from the heart, 
i.e. in the brain, or of clotting in the irregular chambers of the 
heart and propulsion of an embolus thence. 

6. Temperature. — Haemorrhage always causes a fall in the tem- 
perature, which may continue till death or be replaced by irregular 
pyrexia. Plugging of a vessel rarely causes much fall, and, if it 
does so, the temperature soon rises to normal, and continues there 
with very slight or no variation, so that the greater the excursions 
of the thermometer the more do we think of haemorrhage. 

If these various indications are properly balanced, a correct con- 
clusion will more often than not be arrived at, though many mis- 
taken diagnoses will undoubtedly occur. 



3 2o DIFFERENTIAL DIAGNOSIS chap. 

It must not be overlooked on the post-mortem table that a fatal 
plugging may yield no very obvious signs, because the softening 
which we look for as proof of plugging is a phenomenon which 
only commences some little time after the circulation through the 
part has ceased. It may not be out of place, too, to mention that, 
whether the softening be white, red, or yellow, it is merely an acci- 
dental result of (i) the age of the process; (2) the amount of 
blood or other pigment, or their derivatives, left in the area by 
circumstances of absorption ; it has no special significance suggestive 
of a difference in the pathology of the lesion. 

Idiopathic Affections of Neurons 

Though in no sense of the word idiopathic, there is no other 
connection in which the effects of haemorrhage or plugging can be 
more appropriately placed ; consequently, we must tabulate the above 
heading as follows : — 

1. Secondary to their death by gross violence, whether from 

haemorrhage or plugging. 

2. Idiopathic — 

(a) Acute, usually termed acute inflammation. 
(?>) Chronic, usually termed primary sclerosis. 

1. Of the secondary form but little need be said; it undoubt- 
edly occurs as a sclerosis of a tract, or track, after haemorrhage from 
or plugging of a vessel has destroyed the nutritive mechanism, but 
it adds little or nothing to the clinical picture already portrayed. 
The paralysis, or anaesthesia, or both, and the exaggerated reflexes 
appear rapidly as the result of the death of the neuron ; the subse- 
quent sclerosis merely fixes these in rigid features, and adds certain 
confirmation to a previous diagnosis of organic mischief. 

2 (a). The acute primary affection has its chief, if not its only, 
seat in the neuron cells of the motor areas (nuclei of nerves), at 
any rate this localisation property is so constant that clinically it 
affords one of the strongest points of evidence in favour of the 
particular pathological lesion, i.e. of primary acute inflammation or 
degeneration. We find it most commonly in the spinal cord as 
acute anterior poliomyelitis, the diagnostic points of which have 
already been considered on p. 292, but it must not be forgotten 
that the nuclei of origin of the motor cranial nerves are absolutely 
analogous in function, if not even serially homologous in structure, 
to those of the anterior cornua, and are therefore found to be 



vin DISEASES OF THE NERVOUS SYSTEM 321 

liable to the same affections ; hence an acute bulbar paralysis or an 
acute affection of an isolated cranial nerve nucleus may and does 
occur. Its history will be one of acute {i.e. complete within twenty- 
four hours) onset, accompanied probably by a slight pyrexia ; the 
latter may be so slight or fugitive as to escape observation, and 
hence the disease may resemble at its onset a small haemorrhage or 
softening. The differences in such an acute case will principally 
consist in the following : — 

(a) Although it is possible, yet as a matter of clinical experience, 
the onset rarely is so instantaneous as in haemorrhage. 

{b) There will be at any rate in a few hours after onset an 
almost complete absence of any sensory phenomena. 

(c) In the bulb if the cause of the trouble were a haemorrhage 
or softening, it is almost inevitable but that some limb 
paralysis or anaesthesia should be found, for the vessels 
supplying these motor nuclei do not confine their nutri- 
tive supply to these alone; and we have already noted 
the peculiar precision with which this lesion does pick 
out the motor cells only. 

In the identity of its results upon the peripheral nerve and 
the muscles supplied by it (degeneration and atrophy), it has to be 
separated from purely peripheral lesions ; difficulties arise here more 
in theory than in practice ; nuclear lesions are seldom quite com- 
plete {e.g. of third, seventh, sixth, twelfth, etc.), while peripheral ones 
are specially prone to be so, particularly if the nerve {e.g. the seventh) 
passes through a bony canal. Again, if the peripheral lesion be 
only partial, its causes (meningitis, gummata, tumours, etc.) are 
associated with general symptoms or local phenomena (swelling, 
pain, etc.) of such obtrusiveness as to leave little room for doubt if 
the case be seen in an early stage. In later stages diagnosis will 
be impossible without the history to guide us. 

2 {b). In the chronic form of primary sclerosis of tracts, of 
which the following are the chief types : — 



V 



Tabes dorsalis 

Lateral sclerosis ! 

Progressive muscular atrophy 

Disseminated sclerosis of cord and brain 

Chronic bulbar paralysis of bulb ; 

? Paralysis agitans ") c , 

.. c ./ , D > of brain cortex: 

? Senile tremors 



322 DIFFERENTIAL DIAGNOSIS chap. 

the principal feature which separates them at once from every other 
lesion — except a very slowly growing tumour — is the extreme 
chronicity of the process, so that symptoms are slowly developing 
for many months at least, and often even for years. The extreme 
precision with which this affection, i.e. primary sclerosis, picks out 
certain tracks and strands (except disseminated), is also as marked 
a feature as in the acute form, so that, when combined with chroni- 
city, it leaves little room for doubt, at any rate in advanced cases. 
The individual diseases have already received {supra) sufficient 
attention ; it remains here only to remark on the likeness of the 
process to functional disorders. If we consider the minute patho- 
logical processes underlying the gross sclerosis (the final stage), it 
is easy to see that in the early stages of the trouble we are now con- 
sidering, it is probable that a time will occur in which only function 
will have suffered, and consequently this will be a stage in which 
the greatest difficulties may occur in separation ; in fact, there may 
be, and even probably must be, identity of symptoms with a differ- 
ence only in future progress. Attention may be drawn to p. 297, 
where the differences between disseminated sclerosis and functional 
troubles are discussed. Besides what is there recorded there is only 
the general consideration of the element of time ; this, in the 
beginning of a simple functional trouble, which is not going to 
proceed to sclerosis, is likely to show confusion in many systems, 
as opposed to stress on one system in a case that is going to end 
in sclerosis ; and then, again, later will show a stationary or im- 
proving condition in the former versus a downhill course if the 
fundamental meaning of the symptoms is the starting of a pro- 
gressive process of decay and degeneration. 

Tumours of Brain (and of Cord) 

By their comparative chronicity or comparative acuteness, 
according to the point of view from which we regard them, these 
troubles separate themselves almost conclusively from vascular and 
acute inflammatory lesions on the one hand, and, on the other, from 
chronic idiopathic scleroses. From the latter, too, they are also 
separated by the fact that they are very indiscriminate in the 
pressure they exert : they spare nothing that comes within their 
sphere of influence (hence the predominance in the cord of root 
symptoms). As they affect the cord they will receive no further 
notice, but from their importance in the recent advances of cerebral 
pathology and treatment they must be discussed a little more fully 
as they affect intracranial structures. 



vin DISEASES OF THE NERVOUS SYSTEM 323 

It is common knowledge that the tripod on which their diagnosis 
mainly rests has for its three legs : — 

Headache. 
Vomiting. 
Optic neuritis. 

To these are frequently enough added some specific features 
indicating its locality, and occasionally its precise nature. For the 
former, vide Jacksonian Epilepsy and the Cranial Nerves; of the latter 
it is only necessary to mention a definite history of syphilis, tubercle 
in the choroid or elsewhere, and a primary focus in some organ of 
sarcoma or carcinoma. 

Now, any one of these three legs may be permanently knocked 
away and yet the diagnosis stand, while even two may be removed for 
some time without a complete overthrow of the diagnostic super- 
structure ; but if all three be gone it is only in the rarest of instances, 
and more by inspiration than logic, that we should venture to assert 
that a cerebral tumour was present because of some incidental 
localising suggestions. 

Headache. — Pain in the head, even severe, is such a common 
complaint that not much stress can be laid on this symptom until 
the other common sources of it have been excluded. We may 
say that unless at least one of the other two guiding indications 
were present it would hardly arouse suspicion of a cerebral neoplasm 
(not but that the neoplasm may be there, without our suspecting it), 
except it possessed in rather a marked degree some or all of the 
following features : ( 1 ) very persistent and resistant to remedies, and 
possibly paroxysmal; (2) so severe as to keep the patient awake at 
night ; this should be made a very strong point, as patients vary 
very much in their estimation of the intensity of a headache ; 

(3) located in one, and that perhaps an unusual part of the head ; 

(4) often associated with acute additional pain or tenderness on 
percussing the head in that region (this is commoner in superficial 
tumours, and when definitely present is a valuable localising sign). 

Vomiting. — If of cerebral origin {vide pp. 158 and 1 59) is usually 
stated to be unassociated with much, or any, nausea ; totally inde- 
pendent of food (often attempted with an empty stomach), and of 
a peculiarly forcible (pumping) character ; certainly none of these 
features is absolutely constant, even in the certain presence of a 
tumour, but we may safely say that when a patient makes special 
complaint of vomiting as the chief symptom, and no definite gastric 
or alimentary trouble can be found to account for it, it is imperative 



324 



DIFFERENTIAL DIAGNOSIS 



upon us to examine the fundi oculorum and inquire more particularly 
about the headache. The diseases likely to cause such vomiting 
of remote or obscure origin are tabes dorsalis and Addison's disease, 
neither of which should offer any difficulties in exclusion, at least 
from the possible occurrence of a tumour. 

Optic Neuritis. — Inasmuch as a definite optic neuritis occurring as 
a totally independent disease, apart from any discoverable causation, 
is the very rarest of phenomena, if not absolutely unknown, it 
necessarily follows that if we can establish its certain presence, 
and if we can exclude other causes, we have almost proved to a 
demonstration the presence of gross intracranial mischief of but few 
categories. 

As regards its recognition it cannot be too strongly insisted upon, not 
too often repeated, that severe optic neuritis and other pathological changes 
in the fundus may be present without the slightest voluntary complaint on 
the part of the patient of subjective disturbances of vision, nay more, he 
may deny such even when the direct question is ptit to him, so that the 
ophthahnoscope is absolutely necessary for diagnosis. 

The following is a tolerably complete list of causes of the 
changes found in the fundus, with the main characters of separa- 
tion : — 



Gout, cirrhotic kid- 
neys, albuminuria. 



Specific fevers, ty- 
phoid, e.g. 

Leucocythaemia and 
purpura. 



Embolism of central 
artery. 



Anaemia. 



Haemorrhages, or white atrophic spots, the chief 
feature in the fundus ; the examination of the 
urine, and other evidences of vascular degenera- 
tion, leave no room for mistakes. 

The pyrexia, the rash, and general symptoms too 
well marked ; the neuritis itself may be indis- 
tinguishable. 

Again haemorrhages are the prominent feature in 
the fundus ; examination of blood and en- 
larged spleen in the one case, and haemor- 
rhages in the skin in the other, are sufficient to 
prevent mistakes. 

Changes are in the yellow spot, not in the disc, 
except as atrophy ; arteries and veins small 
instead of large. Loss of sight probably com- 
plete in the eye affected. 

Optic neuritis rare, except in cases of very marked 
pallor ; examination of blood gives certain 
information. I have known even Dr. Jackson 
deceived in such a case, however, and diagnose 
tumour from the headache and optic neuritis 
when they were dependent upon simple anaemia. 



DISEASES OF THE NERVOUS SYSTEM 



325 



Lead poisoning. 



Errors of refraction. 



Tubercle. 



In tumour of ordin- 
ary character, or 
syphilitic or tu- 
bercular, and in 
abscess or men- 
ingitis of any 
causation. 



It is very rare that optic neuritis is the only sign 
of plumbism in a doubtful case ; wrist drop or 
colic, or blue line, nearly sure to be present ; 
occupation or opportunities for absorption 
important. 

This is rather a pitfall in estimating the presence 
of a neuritis than a definite cause of that con- 
dition. They must be carefully excluded as 
the possible causes of visible fundal peculiarities 
before other ones are sought ; and the results 
of their correction noted. 

Visible as small nodules in the choroid ; their 
presence is absolutely conclusive as to the 
nature of a tumour or a meningitis if previously 
doubtful, but they are only rarely present even 
when tubercle is the cause we are seeking for 
certain symptoms. 

The optic neuritis when present has usually no 
distinctive characters peculiar to each (? tubercle 
above), but is very frequently present with any 
of them as very strong evidence of a gross 
diagnosis. 



Such are the principal means we have for a pathological diag- 
nosis in general terms. We have already considered the separation 
of meningitis and also of abscess. The question of the space of 
time during which a lesion is developing its features has already 
been repeatedly alluded to, and so also have those features which 
assist us in forming an opinion as to the precise locality of a 
disturbing factor. The question cannot be pursued farther with- 
out going into very special discussion unsuitable for the present 
work. 



CHAPTER IX 

URGENCY CASES 

Under this heading I propose to discuss the diagnosis of a very 
mixed group of cases with which the daily press has from time to 
time made and kept us familiar under the attractive (?) title of 
" Drunk or Dying," in allusion to the fact that so many of them, 
while ending fatally, have a very close resemblance to the varied 
phases of alcoholism in its numerous stages. 

It is for lack of some definite principles in diagnosis (and treat- 
ment) that so many mistakes have occurred, mistakes from which 
no extrication is possible, and through which more than one medical 
reputation has foundered, and public institutions have had much 
undeserved censure cast upon them. 

We may define the group to which I refer as " Cases in which 
we are called upon — usually in a great hurry — to examine and treat 
a patient in whom sudden and apparently severe illness has super- 
vened, and whom we have not been previously attending, or with 
whose previous history we are at the time unacquainted." This 
last condition is put in to temporarily exclude cases of illness 
which are known to be complicated with sudden storms, though 
the following analysis will show that such are not usually present. 

We will commence with a bare enumeration of the lesions which 
are liable to take place suddenly, or, perhaps more appropriately to 
our subject, are liable to cause sudden symptoms in persons who are 
apparently in perfect health, or at least are able to go about the 
public thoroughfares unattended. They divide themselves fairly 
naturally into groups as follows ; — 

I. Haemorrhage. 
II. Vascular lesions other than haemorrhage. 



chap, ix URGENCY CASES 327 

III. Traumatism. 

IV. Sudden death. 

V. Lesions and conditions of the nervous system. 
VI. Poisoning. 

This is a fairly complete list of " urgency cases." It may seem 
a very formidable one to carry in mind, but in practice it is not so, 
for many cases are self obvious from the first, and early treatment 
can proceed on but very few lines. 

Group I. HEMORRHAGE 

(a) Through breach of skin. e.g. Traumatism, varicose veins, etc. 

(b) Appearing externally e.g. Haematemesis, haemoptysis, epis- 

through rupture of vessel taxis, or haemorrhage from 

internally. rectum. 

(c) Concealed haemorrhage. e.g. Rupture of aneurysm, or of tubal 

gestation, or of a vascular 
organ, especially spleen ; 
haemorrhage into stomach 
without vomiting, or into in- 
testine without appearing in a 
stool. (Cerebral haemorrhage 
is not included in this group, 
as it is brain laceration and 
compression that cause its 
symptoms.) 

From the point of view of a provisional or preliminary diagnosis 
guiding us to first or immediate treatment, this group stands almost 
by itself, and may at once be dismissed rather summarily. Sub- 
divisions (a) and (b) are at once obvious by the blood round the 
patient (if the body has been removed or the blood cleaned up 
there will obviously be some history of such having been done). 
Group (c) offers a little more difficulty, but here it is fair to assume 
that if the haemorrhage is sufficiently severe to necessitate the 
attendance of a medical man, it will be sufficient to cause very 
marked blanching of the face, and faintness, with the small pulse, 
weak or husky voice, and sighing respiration characteristic of a 
severe loss of blood. A ruptured aneurysm, spleen, or ectopic 
gestation is, besides the faintness and blanching, also very likely 
to cause severe local pain, directing attention to the region in 
question. 



328 DIFFERENTIAL DIAGNOSIS chap. 

Group II — Vascular Lesions other than Hemorrhage 

e.g. Simple fainting, angina pectoris. (Blocking of blood-vessels 
is excluded here, as the symptoms entirely depend on the 
locality of the block.) 

A diagnosis of either of these conditions is usually, like that of 
haemorrhage, fairly easy. Either of them may have ended in rapid 
death (a subject of special grouping, vide below), in which case 
let me strongly urge that no diagnosis should be given without a 
complete autopsy. Fainting, if not due to actual haemorrhage {vide 
above), is commonly very transient ; if prolonged, it can only be 
diagnosed as a simple lesion by exclusion of the indications of 
Groups V. and VI. {vide pp. 331, 332). 

Angina, if of any severity (and it is only then that it becomes 
an " urgency case "), will be recognised by the position of the pain 
in the chest, and the fixed attitude of the patient from the fear of 
death on movement. 

Group III. — Traumatism 
The only conditions that can arise from traumatism are — 

(1) The actual injury to limbs or viscera. 

(2) Shock to the nervous system, which may be sufficiently 

severe to cause death. 

(3) Unconsciousness, from — 

(a) Shock, pure and simple, 

(0) The nature or locality of the injury, e.g. of brain. 

(4) Death. 

If the victim is conscious, and thus a history obtainable, no 
difficulties in forming a preliminary diagnosis can arise, and we 
are not here concerned with anything deeper or more accurate, 
the discussion of which indeed involves a whole treatise on trau- 
matic surgery. If, on the other hand, the victim is unconscious 
though not dead (again vide Sudden Death), and no history obtain- 
able from friends or bystanders, the patient must be carefully 
examined for any signs of injury (fractured base of skull, or severe 
crush, bullet wounds, etc.), and then, should nothing be found to 
account for the unconsciousness, the case must temporarily be 
placed as " unconsciousness " amongst the group of nervous lesions, 
and its diagnosis sought by means of the indications given under 



ix URGENCY CASES 329 

that heading. The position of the body, as at the bottom of a 
ladder or stairs, etc., may suggest a fall, but even if the fall be 
proved, it may still be due to epilepsy, apoplexy, etc. The shock 
of traumatism, especially if the latter be not very severe, may 
take the shape of a mental condition closely resembling alco- 
holism {q.v.). 

Group IV. — Sudden Death 

The interest of this group is purely medico-legal. There can be 
no clinical diagnostic problem involved, unless it be to give a warn- 
ing to friends as to the possible sudden death of any patient, so 
that worldly affairs may be put in order in time. It is, however, 
impossible to ignore the condition in an article on " Emergency 
Cases," and so I have inserted the following table, which is but 
slightly altered from Professor Dixon Mann's article in the Lancet 
for June 26, 1897 ; the great assistance of which I wish to acknow- 
ledge. Dr. Mann states that in a case of sudden death one of 
three conditions will be found on autopsy : — 

1. A recognisable disease or condition known to be commonly 

associated with a sudden end. 

2. A recognisable disease, but which is not usually terminated 

suddenly. 

3. No recognisable pathological condition anywhere in the 

body. 
Tabulated and arranged, with a few additions and alterations, 
this first list gives the following : — 

(a) Morbus cordis (in about Valvular disease. 

half the cases. — Mann). Possibly congenital abnormality. 

Atheroma of coronary arteries (with or 
without history of angina pectoris). 

Fatty heart. 

Sclerosis of muscle. 

Rupture of wall of a cavity. 
{b) Haemorrhage. Ruptured aneurysm. 

Ruptured spleen. 

Into pancreas. 

Into brain (apoplexy). 

Into stomach or intestine. 

Ectopic gestation. 

Varicose veins, internal or external. 

Traumatism of a large vessel. 



33Q DIFFERENTIAL DIAGNOSIS chap. 

(c) Asphyxia, with a condition Air, serum, blood, or pus in pleural 

or disease known to pro- cavity. 

duce it rapidly. (Edema of, or membrane in, glottis or 

polypoid growth. 
Pressure of tumour (solid or liquid) on 

larynx or trachea. 
Embolus of air in a vein, or clot in a 

pulmonary artery. 
Blood, or other vomited or swallowed 
foreign body in air passages. 

(d) Miscellaneous group, in Perforation or strangulation of gut, and 

which precise mode of peritonitis. 

death not obvious, Exophthalmic goitre. 

though the morbid con- Addison's disease. 

dition is easily recognis- Nephritis of any kind. 

able, and is known on Pneumonia, especially in old people. 

occasions to cause very Abscess or tumour of brain. 

rapid death. Meningitis. 

Obvious damage to a viscus from trau- 
matism. 



In his second list Professor Mann includes some of the con- 
ditions I have put in the first one, and also the following : — 

Diphtheria, without membrane being the apparent cause ; prob- 
ably neuritis. 

Phthisis, with exhaustion probably. 

Ulcerative endocarditis ; may be signs of septic infarction. 

Pericarditis, with effusion of serum or pus. 

Adherent pericardium, probably with recognisable changes in 
the muscle of the heart. 

Gall-stone colic ) May find the stone in the duct or ureter, 

Nephritic colic j but it may have slipped back or out. 

Gout, especially in corpulent individuals, recognised probably 
by the cirrhotic kidney corroborating the joints or tophi. 

Hydatid tumour, which has ruptured. 

The third list of Professor Mann's I have enlarged by including 
in it several conditions which he has placed in the first and second; 
my reason for so doing is that it is only in very exceptional circum- 
stances that the results of the autopsy are sufficient for a diagnosis ; 
there is required in addition a reliable history of the patient in some 
form, or a witnessing of the last scene. It includes : — 



ix URGENCY CASES 331 

Asthma — possible signs of asphyxia. 

Pertussis — possible signs of asphyxia. 

Overlaying of infants. 

Epilepsy — possible signs of asphyxia ; "} , ., , 

y~i i • "i-ii i 3.nd possioiv 

Convulsions in children ; f 1 h' f 

Spasm of glottis — possible signs of asphyxia ; f , ,° 

(Laryngismus stridulus); ) 

Acute rheumatism — cardiac syncope. 
Zymotic diseases — occasionally by intensity of the poisoning — 

without a rash. 
Hyperpyrexia — sunstroke, acute rheumatism, etc. 
Influenza. 
Excitement or fright as in quarrelling, or near approach of any 

danger — thought of an operation, etc. 
Chronic alcoholism — probably some neuritis of pneumogastric. 

On these lists I do not propose to say anything further ; their 
importance is'obvious and enormous ; but when we have admitted 
the fact of sudden death, and have made a thoroughly careful post- 
mortem, clinical medicine ceases its functions, and legal procedures 
come to the front with all the available evidence as to what was 
happening, or had just happened, when death took place. 

We now come to the two groups which include the real 
crux of the position, and are the essential clinical elements in 
drunk or dying. They must be considered in some considerable 
detail. 



Group V. — Lesions and Conditions of the Nervous System 

Cerebral plugging or rupture of a vessel, constituting apoplexy 

of the laity. 
Epilepsy — including post-epileptic states, and also malingering 

of fits. 
Hysteria. 

Plumbism — lead encephalopathy. 
Lunacy — especially G.P.I. 

Cerebral tumour — with epileptiform convulsions. 
Sunstroke. 
Meningitis, and acute encephalitis. 

(Simple fainting will be here considered; as its main symptom 
is apparently cerebral.) 



332 DIFFERENTIAL DIAGNOSIS 



Group VI. — Poisoning, including two Sub-Groups 

A. Autogenetic. Uraemia. 

Diabetic coma. 

B. From without, which may include any and every poison, 

however administered, but from our present point of view 
has especial reference to — 

Alcohol. 

Opium and other narcotics, such as chloral. 

Belladonna as a deliriant. 

Strychnia as a convulsant. 

Both for diagnosis and treatment it will be well to maintain a 
chronological order of events, as this will render the discussion 
much more practical, even if it introduces a little theoretical incon- 
sistency. 

Commencing then with the history. While getting ready to go 
or going with the messenger we must inquire into the particulars of 
the seizure as closely as possible : asking, for instance, Has the patient 
taken anything ? — if so, Of what known nature ? — Whence obtained ? 
— Is he in a fit ? etc. From the answers to these questions, if they 
be intelligent or even intelligible, valuable hints may be obtained. 
I am bound to admit that in the majority of cases there will be 
either no history at all, owing to the absence of witnesses, or the 
history will be unintelligible, owing to the anxiety, fright, or imbe- 
cility of the messenger ; or, again, it may be purposely misleading 
in some few criminal cases. Such as it is, however, listen to it, 
and use your own judgment as to its value. 

On arrival, the first thing is to clear the room or a space round 
the individual, to give him air, to prevent bystanders doing mis- 
chief, and to enable you to exert your own efforts without unneces- 
sary interruption. Secondly, while doing this, you will have a few 
moments in which to note the general aspect of the patient. Is he 
motionless and apparently dead, or is he in a fit, convulsed and 
obviously living ? Is his face natural in colour, or is it blue with 
livid lips, and is froth issuing from them ? — if so, Is the froth blood- 
stained ? Is he sweating profusely, or is his face dry ? Thirdly, 
while noticing these facts loosen everything from the neck, cutting 
the clothes if necessary for rapid action to prevent imminent 
asphyxia. And lastly, if convulsed, restrain him in some way, so 
as to prevent him from injuring himself by the violence of his 
movements. 



ix URGENCY CASES 333 

We are now in a position to take diagnosis into consideration, 
and this obviously proceeds in two directions, according to whether 
the patient has convulsions and is living, or whether he is quiet and 
possibly dead. 

If he is in a " fit," this may be due to — 

Cerebral (haemorrhage, tumour, etc.) ; 

Epilepsy ; 

Hysteria ; 

Malingering ; 

Poisoning — strychnine especially, but possibly opium or other 

poison ; 
Uraemia ; 

Dentition, etc., in babies; 
Tetanus ; 

and the following are the points most worth attention to decide 
which of these is present. 

1. Age and Sex. — Of age little need be said, for at all ages 
many things are possible. It is obvious that dentition can only 
occur in babies, and in these young subjects convulsions are very 
common from every form of reflex irritation ; the precise cause can 
only be cleared up by the same careful examination as in adults ; 
the condition, though very common, hardly gives rise to difficulties in 
our present connection,/.*?, with "urgency." Sex, too, has only 
this influence, that in females, and especially from seventeen to forty 
years of age, we lean more strongly to a diagnosis of functional 
trouble of no great immediate danger. 

2. The Eyes. — A most, perhaps the most, important seat of 
clues. 

Are they open or shut ? — if shut, Is there much resistance to your 
opening them by lifting the lids? — Is the patient looking round 
furtively ? This furtive glancing and resistance to opening the eyes 
is very suggestive indeed of hysteria or malingering. Then the state 
of the pupils, note are they equal or unequal, dilated or contracted, 
do they react to light or not, is the conjunctival reflex present. In 
epilepsy the pupils are dilated and insensible to light, or occasionally 
oscillating without obvious cause : in hysteria they react readily to 
light, and in malingering (unless artificially tampered with) they will 
obviously do the same. In poisoning they will usually not act to 
light, if it be by strychnine, the only likely convulsant, they will be 
dilated, as will also happen if asphyxial convulsions are due to some 
poison; should it happen to be a case of opium poisoning with 



334 DIFFERENTIAL DIAGNOSIS chap. 

convulsions they will be contracted. In uraemia the pupils are as a 
rule fixed and dilated, they react very slowly, if at all, to light, but it 
may happen that they are of natural size. If the pupils are unequal 
we shall think of pontine or other cerebral haemorrhage, or of 
general paralysis of the insane. The conjunctival reflex will be 
absent in epilepsy, uraemia, and other more dangerous conditions ; 
certainly present in hysteria and malingering. 

We may sum up the matter by saying that if (i) fixed (small or 
large), or (2) irregular and unequal, pupils are present, or if (3) the 
conjunctival reflex is absent, then the condition is serious, and may 
be a dangerous one. If, on the other hand, the pupils react readily 
to light, it is probably a less serious matter, and if the conjunctival 
reflex is present this adds greatly to the probability of a recoverable 
condition. 

3. Froth coming from Month. — This is usually present in 
epilepsy, and very possibly blood-stained from biting of the tongue. 
If it be blood-stained, epilepsy is certainly most probable in the 
absence of motive for malingering. Malingerers will use soap for 
froth-making purposes, so that the mouth must be examined for this 
article. Froth may be present in poisoning, but has then no special 
significance except as suggesting hydrocyanic acid, but then fits are 
not present. 

4. Note the Nature of the Convulsions. — They are most exag- 
gerated perhaps in hysteria, and most universal. The malingerer is 
apt to over- or under-do the movements. In poisoning by strych- 
nine an attack is soon over and followed by complete relaxation of 
muscles ; in tetanus this relaxation is incomplete ; moreover strych- 
nine convulsions are more marked in head and trunk (opisthotonos 
or emprosthotonos), while tetanus is more likely to be concentrated 
in the jaws and neck. In epilepsy, too, opisthotonos is usually 
absent, and malingerers cannot keep it up for long, even if they can 
assume the position at all. In cerebral haemorrhage or blocking 
with convulsive movements, these will take the shape of conjugate 
deviation of head and eyes, a most important sign, hardly ever met 
with except with such gross lesion. 

5. The Ge?ie?-al Appearance of the Face. — In malingerers certainly, 
and usually in hysteria, the face is hot and flushed, and the body as 
well bathed in hot perspiration (note the state of the weather or 
atmospheric pressure) if the movements are at all violent. In epi- 
lepsy the face is possibly blue and congested, or more probably 
pale ; it may be moist, but it will be with a cold sweat, and the 
same coldness will be present in poisoning. In uraemia the face 



ix URGENCY CASES 335 

may be flushed, but it is more usually natural or pale without 
sweat. 

6. The General Consciousness and Capability of being Roused to 
Speech. — In malingering and hysteria he can certainly be roused ; 
in epilepsy and uraemia he cannot be ; in poisoning he is either 
totally unconscious (hardly in this group), or is perfectly conscious 
and rational between the fits. 

7. The Pulse. — Over this the patient can have no control. In 
malingering and hysteria the pulse will be full, bounding, and rapid 
from exertion. In uraemia and poisoning it is likely to be very 
small and rapid ; in epilepsy it is usually somewhat accelerated ; in 
gross cerebral lesions it is likely to be very slow, from cerebral com- 
pression. 

Such are the most important means of immediate or rough 
diagnosis, none of them individually trustworthy ; each has to be 
considered in relation to the others. I do not propose to consider 
the more accurate diagnosis any further, as the main object of this 
chapter is to draw a line between those cases for which a bucket of 
water or a police cell is advisable, and those for which skilled 
medical attention in a place of rest and quietude (bed at home, or 
in a hospital) is the only safe line to pursue. 

We will now pass on to the second group of cases, viz. those in 
which convulsions with (genuine or feigned) unconsciousness are not 
present. Here the cases may be divided into three classes, though 
I shall speak of them only in two : — 

I. — Those who are actively conscious (this consciousness may be 
very perverted in its judgment), and perhaps noisy and abusive, 
especially when undergoing physical examination. 

II — Those who are unconscious, but can be roused by speaking, 
pinching, pricking, etc. 

III. — Those who are absolutely comatose, and cannot be roused 
at all. 

Firstly, then, those who are actively conscious and may be noisy. 
Practically there are four things to be thought of here : — 

(1) Alcoholism — drunkenness; 

(2) Head injuries and cerebral disease; 

(3) Lunacy; 

(4) Poisoning other than alcohol — rarely ; 

and it must never be forgotten that the first may be combined with 
any of the others ; a complication the possibility of which forms the 
principal crux of the problem. 



336 DIFFERENTIAL DIAGNOSIS chap. 

Here again, the first thing is the history from others or from the 
patient, and it is very probable that in this class of cases it will 
throw strong light on the diagnosis, especially when taken with the 
manner in which it is told. 

Lunacy, under these particular circumstances, is almost sure 
to betray itself either by the absolute nonsense the patient talks, or 
by the direct contradiction of, or lack of confirmation from, the 
story of those with him. The manner of relating his tale differs 
materially. in the lunatic and the "drunk." The lunatic may relate 
his tale perfectly quietly and with pseudo- rationality, the drunken 
man is nearly sure (in this stage) to be very excitable and inco- 
herent : the speech of the former will be complete in its individual 
words (except in general paralysis of the insane, when the long words 
may be slurred), that of the latter will have the easily recognised 
character of drunken speech. 

If actual lunacy can be excluded, but we have a strong suspicion 
that alcohol has been at work with or without an accident of some 
kind, the tale of others may be of most material value. In cases of 
head trouble, whether from traumatism (shock is here an important 
element) or from disease, a little alcohol goes a long way, so that if 
there be the slightest suspicion of serious trouble, abuse and noisi- 
ness must be largely discounted, and the patient taken under pro- 
fessional care. A case in point occurred within my experience some 
years ago. The patient was at first quiet, but began to be noisy, 
abusive, and very pugnacious when examined. He was thought to 
be drunk, and was on the point of being sent away when another 
house physician saw him, thought he looked very ill and peculiar, 
and advised his admission to the wards : he died before reaching 
them, and the autopsy showed that it was a case of cerebro-spinal 
meningitis. See, therefore, how noisy and abusive conversation fits 
in with other facts in the history. 

If what you hear is not sufficient, see what you can ascertain 
with your eyes. The colour and appearance of the face may help. 
In alcoholism it will be flushed ; in head mischief, whether haemor- 
rhage or inflammation, the face is possibly flushed, but it is much 
more likely to be pale, or blue and congested — bloated ; in a lunatic 
the face will seem natural, or possibly flushed with exertion ; in 
deliriant poisoning the face will be dry and flushed, or cold and 
clammy. The condition of the pupils is as important here as in 
the case of convulsions ; in alcoholism they are sure to be dilated, 
and probably fairly active ; indeed, if the patient is not comatose 
from alcohol they are sure to be active. In head conditions, 



ix URGENCY CASES 337 

though the pupils may be active, they are more likely to be fixed, 
dilated, contracted, or unequal, or at least sluggish in movement. 
In lunatics (except general paralysis, when they are unequal or 
sluggish) they are active enough. In poisoning in this stage they 
would be widely dilated and inactive, with brightly glistening eyes. 

If still in doubt the temperature should be taken. This in 
serious cases is pretty sure to be markedly raised or lowered. If a 
normal temperature is found in a man who is actively conscious, or 
can be roused very easily, and if at the same time his pupils are 
active, the probabilities are that there is nothing very serious the 
matter. If, on the other hand, the temperature is raised, inflam- 
matory conditions must be suspected, either in the brain or possibly 
elsewhere (unsuspected pneumonia, e.g.), and if markedly lowered 
we know that there is a depression likely enough to be or become 
dangerous, and the case had better be watched. 

These points, if carefully considered, will be, as a rule, sufficient 
to prevent serious mistakes, but keep all your faculties on the stretch 
for any little suggestive point ; finally, if in doubt, act as if the case 
were a serious one. 

We will now pass on to the other group of cases — those in 
which the patient is quiet and actually unconscious, though he may 
be capable of being roused momentarily. 

There is here only one golden rule of treatment : Never allow 
an unconscious patient to be left alone. If he is seen at a 
hospital take him in. Far better to take in fifty drunken men in 
one night, and let them lie on mattresses under supervision in a 
warm room, than let one die unattended. The one action can at 
the worst only subject you to mild chaff and cause temporary incon- 
venience, the other may ruin you or your hospital for ever. If seen 
elsewhere than at a hospital have him removed at once to a hospital 
or to his home (or some one else's), and do not leave him till some 
reliable person is in charge. This is a golden rule, from which no 
possible concurrence of circumstances should ever allow you to 
depart. 

Accurate diagnosis is therefore, from the point of view of imme- 
diate treatment, but of little use, but for further treatment, and for 
our reputations' sake, we must endeavour to make one. 

Any one of the conditions hitherto enumerated in this chapter 
may be present, or a combination of two or more. A drunken man, 
for instance, is not absolutely free from the chance of being injured 
by blows or falls, and he is even more likely than a sober one, 
ceteris paribus, to have an intracranial haemorrhage, for if a man's 

z 



33S DIFFERENTIAL DIAGNOSIS chap. 

vessels are diseased and he gets drunk, the arteries, which can do 
so, dilate, the diseased ones cannot, and rupture may occur. A 
hysterical woman may have a genuine epileptic fit with post-epileptic 
coma, and she may have got drunk previous to either, and finally 
have been damaged. 

Your preliminary actions are here the same as in the other 
groups. Clear a space round the patient, free his neck, listen to 
any history that is forthcoming, and if definitely pointing to poison 
act promptly on it. Do not forget that coma from alcohol is as 
much poisoning by that substance, and often as dangerous, as is 
poisoning by opium or any other drug. 

Smell the Breath. — In the absence of a definite reliable history 
(either of an alcoholic bout or of only one glass given by anxious 
friends) the smell of alcohol is of equal importance with the smell 
of other poisonous substances. If a definite history is forthcoming 
an alcoholic smell must be judged by it. 

Camphor, turpentine, carbolic acid, hydrocyanic acid, chloro- 
form, aether, opium are the principal commoner poisons that will 
have imparted a distinctive odour to the breath. In diabetic 
coma the breath will be sweet like apples. Lately, on entering a 
patient's bedroom, I thought I had gone by mistake into an apple 
storeroom. Occasionally patients in uraemic coma are said to 
smell of ammonia. 

Note the Face as Before. — If it is pale and dry the case is quite 
likely to be only simple fainting, if there are no other distinctive 
symptoms ; if it is pale and sweaty, with cyanosed lips, cerebral 
haemorrhage or poisoning are most probable ; if flushed brightly 
it may be alcohol or belladonna poisoning, or possibly fever ; if 
the face be purple and bloated, this points almost conclusively to 
serious cerebral mischief, probably compression. 

Next Proceed to Examine the Pupils. — In the other sections we 
have already considered the broad outlines of the conclusions to 
be drawn from the condition of the pupils. We may here finally 
tabulate the possible conditions, with a few remarks on their special 
influence on final diagnosis. 

The pupils may be — 

As regards As regards As regards 

Reaction to Light. Absolute Size. Relative Size. 

Active. Dilated. Equal. 

Sluggish. Normal. Unequal. 

Totally inactive. Contracted. 

And finally either one or both may be irregular in outline. 



ix URGENCY CASES 339 

Conditions in which the Pupils are still Active. — This is only 
likely to be the case when the condition of the brain causing the 
unconsciousness is either of a temporary character or in a very 
early stage. Inasmuch as we can but rarely see the patient in 
the latter condition, it is almost a fair clinical deduction to say 
that still very active pupils indicate no immediate danger. Thus 
they will be found in malingerers, in simple fainting (then indica- 
tive of returning consciousness), in hysterical and cataleptic con- 
ditions, and in the later stages of post-epileptic coma that is not 
going to prove fatal. The malingerer may be aware that he can, 
by stimulating the palm, dilate the pupil on that side, but this 
is such a temporary phenomenon as to cause little or no difficulty. 
In poisoning the pupils are frequently unaffected in the early stages, 
but this can hardly occur when absorption has so far advanced as 
to cause coma. The absolute size of active pupils will depend 
upon the amount of light in the examination room 

Conditions in which the Pupils are Sluggish 

This occurs in — 

General paralysis of in- They will probably also be unequal, and 
sane. behave otherwise in a bizarre manner, 

possibly dilating with light. 

Uraemia. May be small, natural in size, or dilated. 

Disseminated sclerosis. In any condition, like uraemia. 

Early stages of apoplexy. Will probably cease to act before the ex- 
amination is completed. 

Conditions in which the Pupil ceases to React to Light at all 

The first and most important deduction from this state of the 
pupils (if we can exclude a glass eye and previous total blindness) 
is that the condition of brain underlying it is very serious, and even 
likely to prove fatal ; it marks the dividing line between coma and 
stupor. 

The commonest examples are : — 

Pupils very small. Opium poisoning (very rarely dilated). 

Pontine haemorrhage (also often unequal). 
Possibly in general paralysis of the insane, or in 
tabes dorsalis. 
Pupils large and Belladonna (and its allies) poisoning, and also in 
equal. the later stages of most poisons, especially if 



34Q DIFFERENTIAL DIAGNOSIS chap. 

asphyxia Is or has been a prominent feature. 
In connection with the large pupils of alcoholic 
poisoning it is worth while to note that even 
in a condition of coma due to this cause the 
pupils will still react to powerful peripheral 
stimuli, such as pinching the patient or pulling 
his hair forcibly. I know of no other grave 
condition of which this can be said. 
Pupils unequal. Frequent in one-sided pontine lesions. Also in 

one-sided considerable increase in intracranial 
pressure, as from haemorrhage. 
In general paralysis, too, it may continue during 
a final coma if previously present. 

After the examination of the eyes look for localised paralyses 
anywhere. Is the face reasonably symmetrical ? Are the eyes in a 
natural axis or markedly deviating ? Do the arms or the legs drop 
equally powerlessly when raised ? 

A localised paralysis of this sort is almost pathognomonic of 
coarse cerebral lesion, but of course in deep coma the point is often 
difficult to appreciate. 

The next point is the respiration. If this is stertorous the 
probabilities are in favour of a cerebral lesion ; but one must not 
forget that it may become stertorous in every form of dangerous 
coma. 

Then the pulse. If it be small, compressible, and slow, it is 
very likely to be opium poisoning (occasionally opium produces a 
very rapid pulse) or pontine lesion. If it be small and thready and 
rapid, no conclusion can be drawn, as this pulse is met with in so 
many conditions of coma where death threatens. A slow, labouring 
pulse, especially with a thickened artery, is suggestive of cerebral 
haemorrhage, or post-epileptic coma. 

Now draw off some of the urine. If sugar be present, diabetic 
coma is rendered probable though it occurs when anything presses 
on the fourth ventricle ; e.g. I have found it in cerebellar haemorrhage. 
If it is ursemic coma, there is likely to be albumen, or possibly blood, 
or both, and the urine will be of low specific gravity ; this latter is 
especially important, as the urine of cirrhotic kidney often enough 
contains no albumen, or such a faint trace as to be easily 
overlooked. A cirrhotic kidney, too, renders haemorrhage very 
likely. 

After noting the foregoing points, try how far thepatient is capable 
of being roused ; the danger increases pari passu with the depth of 



ix URGENCY CASES 341 

the coma. In uraemia, even when likely to prove fatal, some signs 
of consciousness can usually be obtained by pretty forcible stimula- 
tion ; this forms a valuable — not conclusive — distinction between 
uraemia and the coma of cerebral haemorrhage. 

Lastly, take the temperature. This may give some information ; 
it will be very high in sunstroke or other forms of heat apoplexy, 
and gives instantly the best guide to treatment. It almost certainly 
will be raised in the comatose condition of general paralytics, or of 
inflammatory conditions, and hence will be of great use in separating 
these from haemorrhage, uraemia, etc., in which the temperature (at 
the time we are considering) is invariably subnormal. 

In conclusion, I must again repeat that no one of these indica- 
tions is sufficient by itself; all must be considered and a balance 
struck. The history may be absolutely conclusive, and now and again 
an individual feature (e.g. conjugate deviation) may be so marked 
and obtrusive as to outweigh everything ; but whatever conclusion 
we finally arrive at, we must never leave a comatose patient 

WITHOUT EFFICIENT SUPERVISION ; HE MUST ALWAYS BE WATCHED 
CAREFULLY TILL A SUFFICIENT TIME HAS ELAPSED TO ALLOW OF 
AN ALCOHOLIC COMPLICATION HAVING PASSED OFF. 



- 



INDEX 



Abdomen, pain in, vide Colic 

physical examination of, 168 

Abortive zymotics, meaning of, 31 
Abscess, of lung, foetid sputum in, 56 

v. tumour, of brain, 316 

Acid, uric, 209 

Addison's disease, pathology of, 23 
Adenoids as cause of epistaxis, 149 
Adhesions as cause of abdominal pain, 

63 
Age and chronic bronchitis, 99 

and disease, 12 

and tubercle, 238 

in hemiplegia, 318 

old, shortness of breath in, 58 

Ague v. ulcerative endocarditis, 145 
Air in pleura, causes of, 80 
Air-tubes, pressure effects on, 59 
Albuminuria, 195 

cyclical or functional, 196 

eye changes in, 324 

treatment of, 199 

Alcoholism, coma in, 338 

inco-ordination in, 269 

in urgency cases, 336 

peripheral neuritis in, 283 

pupils in, 336, 340 

shock in, 329 

tremors of, 311 

Anaemia, cardiac bruits in, 129 

eye changes in, 324 

nervous phenomena in, 273 

respiration quickened in, 57 

Anaesthesia, paradoxical, 282 
Anchylostomiasis, 156 
Aneurysm as cause of colic, 173 

as cause of pressure, 61 

bruits of, v. valvular disease, 132 

pain in, 61 

pressure of, on cord, 290 

thoracic, 107 



Aneurysm, treatment of, 134 

v. growth in thorax, 107 

Angina pectoris as urgency case, 328 

Antitoxin, arguments for existence of, 5 

in diphtheria, 39 

special or general, 6 

Anuria, causes of, 217 

Anus, blood appearing at, 156 

diseased conditions of, 176 

Aphasia, motor, 305 

Apoplexy and sudden death, 331 

Appendix and pain, 173 

Arsenic, peripheral neuritis from, 283 

Arteries, pressure on, in thorax, 59 

Arterioles, degeneration of, in emphy- 
sema, 99 

Arthritic diathesis, the, 244 

Arthritis, rheumatoid, z\ true rheumatism, 
242 

Ascites, 177 

causes of, 178 

purulent, 179 

tapping v. incision for, 179 

v. encysted fluid, 181 

Asphyxia and sudden death, 330 

Ataxic paraplegia v. peripheral neuritis, 
295 

Ataxy, locomotor, vide Tabes Dorsalis 

Athetosis, 311 

Atrophy, progressive muscular, v. peri- 
pheral neuritis, 293 

Auscultation of chest, 69 

Bacteriology, principles of, 25 
Ballooning of rectum, 176 
Barometer, living, meaning of, 243 
Bell sound on percussion, 73 
Bile in sputum, 55 

in urine, tests for, 190 

Bladder, causes of pus from, 202 
haemorrhage from, 204 



344 



DIFFERENTIAL DIAGNOSIS 



Bladder like rectum, 265 

reflexes of, 263 

Blood dyscrasiae as cause of nerve 

symptoms, 273 
Blood from kidneys v. from bladder, 203 

in urine, 203 

Blood-spitting, causes of, 54 
Bone, features of pain from, 60 

pressure on, in thorax, 60 

Brain, abscess of, v. tumour, 316 

acute vascular lesions of, 315 

difficulties in studying, 306 

diseases of, 306 

haemorrhage into, v. meninges, 317 

effect of heart failure on, 119 

functions of, 255 

localisation in, 307 

peduncles, affections of, 298 

softening of, P.M. table, 320 

softening of, v. haemorrhage, 318 

softening of, varieties of, 320 

tumours of, 322 

tumours of, headache in, 323 

v. cord, lesions of, 279 

white matter, functions of, 308 

Breath, foul, v. foetid sputum, 56 

shortness of, in heart disease, 113 

shortness of, in old people, 58 

shortness of, v. dyspnoea, 58 

smell of, in urgency cases, 338 

sounds, 69 

Breathing, cavernous, 72 

diaphragmatic, 58 

Bright's disease, 217 
Bronchiectasis, 99 

foetid sputum in, 56 

sputum in, 53 

Bronchitis, acute, and bronchopneu- 
monia, 97 
Bronchitis, acute, and uraemia, 216 

acute, cough in, 50 

acute, temperature in, 48, 98 

acute, v. tubercle, 91 

capillary pyrexia in, 48, 100 

chronic, and its associations, 98 

chronic, and phthisis, 94 

chronic, complications of, 99 

chronic, blood-spitting in, 54 

Bronchopneumonia and tubercle, 100 

and chronic bronchitis, 100 

pyrexia in, 98 

pyrexia in, v. bronchitis, 48 

v. tubercle, 91 

Bruits, exocardial v. endocardial, 127 

haemic v. organic, 129 

importance of, 116 



Bruits of aneurysm, 132 

valve of origin of, 130 

vital significance of, 133 

Bulbar paralysis, 321 

v. haemorrhage, 321 

Bulging of chest, 66 
Bursas, enlargement of, 233 

Calcium phosphate in urine, 208 
Capsule, internal, functions of, 308 
Carcinoma of kidney v. stone or 

tubercle, 224 
Caries affecting spinal cord, 290 

as cause of chest pain, 61 

as cause of colic, 173 

Case taking, instructions for, 2 

Casts in urine, 205 

Cavernous breathing, 72 

Cavity in lung, signs of, 84 

Cells of body, disturbed functions of, 15 

of body, disturbed functions in 

blood-poisoning, 16 
Cells of nervous system, affections of, 320 
Cerebellum, functions of, 307 

inco-ordination from, 269 

Charcot's joint, 231, 232, 235, 240 

Chemiotaxis, definition of, 29 

Chest, comparison of two sides of, 64, 

65 
Chest, inspection of, 65 

oedema of, 66, 108 

pain in. 61 

palpation of, 66 

tumour of, 66 

veins enlarged on, 66 

wall, bulging of, 66 

Cheyne-Stokes breathing, 58 
Children, cholera nostras in, 43 
Cholera, asiatica v. nostras, 43 
Chondroarthritis, 239 
Chorea a cortical trouble, 311, 314 

and traumatism, 312 

Choroid, tubercle in, 325 

Clicky crepitations, 92 

Cogwheel respiration, 72 

Cold and cough, origin of phthisis in, 92 

Colic, 161 

and sudden death, 330 

causes of, 161 

differential diagnosis of, 163 

renal, v. biliary or intestinal, 171 

simple v. obstructive, 169 

with collapse, points in, 165 

with collapse, operation in, 165 

without collapse, 167 

Coma in alcoholism, 338 



INDEX 



345 



Coma in uraemia v. cerebral haemorrhage, 

Coma, temperature in, 341 

v. stupor, pupils in, 339 

Communicable v. infectious, 24 
Comparison of two sides of chest, 64, 65 
Compensation in heart disease, 120 
Concussion, 318 
Congenital disease, 12 
Consciousness in hemiplegia, 319 
Constipation and diarrhoea, 173 

consideration of, 175 

Contagion v. infection, 24 
Convulsions, nature of, in urgency cases, 

334 
Convulsions v. rigors, 95 
Co-ordination of motion, 268 

of sensation, 258 

Cord, spinal, continuation of, into 

medulla, 299 
Cord, spinal, diseases of, 285 

function of, general, 255 

function of systems of, 286 

gummata of, 290 

lesions of, indiscriminate, 290 

lesions of, irritative v. destructive, 

290 
Cord, spinal, lesions of, system, 285 

meningitis of, 290 

pressure of aneurysm on, 290 

syphilis of, 290 

v. brain, 279 

Corona radiata, 308 
Corpora quadrigemina, 309 
Corpus callosum, 308 

striatum, 308 

Cough, at night, 52 

classification of, 49 

in ear trouble, 50 

in heart disease, 113 

in laryngeal trouble, 50, 77 

in thoracic tumours, 51 

useless, causes of, 50 

Coughing during auscultation, 84 
Cranial nerves, 303, 305 
Crepitations, clicky, 92 

definition of, 70 

Cyst, abdominal, v. ascites, 181 

Damage, old, and elasticity of function, 

60 
Death, sudden, causes of, 329 
Defalcation and micturition, 265 
Degeneration as process of disease, 16 

causes of, 17 

reaction of, 269 



Degeneration, secondary, 17 
Delirium, 276 
Desquamation, point in, 36 
Diabetes, insipidus, 227 

pathology of, 213 

peripheral neuritis in, 283 

phosphatic, 227 

Diagnosis, definition of, 1 

second stage in, 4 

three stages in, 1, 5 

Diaphragmatic breathing, 58 
Diarrhoea and constipation, 173 

and constipation, causes of, 173 

and uraemia, 216 

considerations in case of, 174 

in phthisis, 94, 177 

severe, v. cholera, 43 

Diathesis, 13 

arthritic, 244 

Diet and disease, 10 
Dilatation of heart, 120, 121 
Diphtheria and antitoxin, 39 

as cause of epistaxis, 149 

paralysis in, v. infantile paralysis, 

295 
Diphtheria, peripheral neuritis in, 283 
— — v. hospital sore throat, 39 
Disease, abortive, meaning of, 31 

and diet, 10 

and new growths, 13 

causes of, 6 

congenital, 12 

processes of, 13 

reasons for thinking it microbic, 29 

Disseminated sclerosis v. peripheral 

neuritis, 296 
Drunk or dying, 326 
Dullness on percussion, degrees of, 67 
Duodenum, ulcer of, 156 
Dying or drunk, 326 
Dyspepsia v. heart pain, 32 

v. gastric ulcer, 182 

Dyspnoea v. shortness of breath, 58 

Ear, cough from, 50 
Eburnation of bone, 240 
Effusion, pleuritic, 102 

pleuritic, and pleurisy, 101 

Elasticity, definition of, 12 
Embolism, eye changes in, 324 

of mesenteric artery, 161 

Emphysema, 99 
Empyema, sweating in, 48 
Endocardial v. exocardial bruits, 127 
Endocarditis, pathology of, 141 
types of, 142 



346 



DIFFERENTIAL DIAGNOSIS 



Endocarditis, ulcerative, 141 

— — ulcerative, diagnosis of, 144 

ulcerative, v. ague, 145 

ulcerative, v. tubercle, 145 

ulcerative, v. typhoid, 144 

Enuresis, 264 

Environment and disease, 10 

Epilepsy, 276 

as urgency case, 333 

Jacksonian, 309 

Jacksonian, v. idiopathic, 310 

nocturnal haemorrhage in, 151 

pupils in, 333 

Epistaxis, causes of, 149 
Erythema simplex v. other rashes, 43 
Etiology as part of pathology, 22 
Exanthemata v. infantile paralysis, 292 
Exercise, influence of, on urine, 186 
Exocardial v. endocardial bruits, 127 
Eyes, the, inco-ordination from, 269 

the, in "fits," 333 

the, in anaemia, purpura, gout, 

cirrhotic kidney, albuminuria, fevers, 

leucocythaemia, 324 
Eyes, the, changes in fundi, in plumbism, 

refraction errors, tubercle, tumours, 

3 2 5 

Face, the, in coma, 338 

the, in urgency cases, 334 

Faeces, points in examination of, 175 

rectum full of, 1 76 

Fainting as urgency case, 328 
Fat as alterer of physical signs, 66 
Fever, eye changes in, 324 

symptoms of, 35 

Fibroid phthisis, origin of, 91 
Fits, causes of, in urgency cases, 333 
Flat foot, 235 
Fcetor of sputum, 55 
Food, influence of, on urine, 187 
Foot, flat, 235 
Fremitus, tactile, 66 

Frequency of micturition, causes of in- 
crease in, 188 
Friction sounds, pleural, 73 
Frontal lobes, function of, 307 
Froth at mouth in urgency cases, 334 
Function of cells in disease, 14, 15 
Functional nerve troubles v. sclerosis, 322 
nerve troubles v. organic, 275 

Ganglia, basal, of brain, 308 
Gangrene of lung, fcetor in, 56 
Gas in pleura, 81 
Gastritis v. meningitis, 160 



Giddiness and uraemia, 216 
Girdle pain, 288 
Glycosuria, 212 

Gonorrhceal rheumatism, 235 ■ 
Gout, 233 

changes in fundi oculorum in, 324 

in joints, 238 

pathology of, 210 

peripheral neuritis in, 283 

G. P.I. , tremors in, 311 
Granulomata, inflammation in, 87 
Grating in joints, 231 
Growths as cause of disease, 13, 18 

intrathoracic, and pressure, 61 

intrathoracic, v. aneurysm, 106, 

107 
Gummata and cranial nerves, 321 
Gums, haemorrhage from, 151 

Haematemesis, causes of, 154 

v. haemoptysis, 152 

Haematuria, 203 
Haemic v. organic bruits, 129 
Haemophilia as cause of epistaxis, 149 
Haemoptysis, causes of, 54, 153 

in chronic bronchitis, 100 

its indications, 92 

v. haematemesis, 152 

Haemorrhage and sudden death, 329 

and tumours of brain, 314 

brain v. meninges, 317 

from mouth, causes of, 150 

from nose, 148 

into tumours, 272 

in urgency cases, 327 

v. acute bulbar paralysis, 321 

Headache and uraemia, 216 

in cerebral tumours, 323 

Heart and pericardium, diseases of, 112 

bruits, exocardial v. endocardial, 

127 
Heart bruits, importance of, 116 

bruits, organic v. haemic, 129 

bruits v. sounds of like nature, 126 

dilatation of, 121 

disease, age in, 138 

disease and epistaxis, 150 

disease and sudden death, 329 

disease, cough in, 51 

disease, general symptoms of, 117 

disease, local signs of, 113, 114 

disease, nervous v. muscular, 137 

disease, pain in, 61 

disease, sex in, 139 

disease, without bruits, 135 

enlargement of, diagnosis of, 122 



INDEX 



347 



Heart, failure of, 118 

failure of, as cause of disease, 18 

failure of, character of sounds in, 

124 

Heart, failure of, definition of, 120 

hypertrophy of, 120 

hypertrophy of, diagnosis of, 122 

hypertrophy of, symptoms of, 121 

its functions, 117 

natural sounds of, 115 

organs, 118 

pressure on, 59 

regularity of, 115 

state of, in hemiplegia, 319 

valvular lesions, effects of, 125 

valvular lesions, influence of indi- 
vidual, 134 

Heat in joints, 233 

Hemianaesthesia, 308, 311 

Hemianopsia, seat of lesion in, 303 

Hemiplegia, diagnosis of seat of lesion 
in, 302 

Hemiplegia, heart in, 319 

softening v. haemorrhage, 318 

temperature in, 319 

— — Trousseau on, 319 

Heredity and disease, 12 

in tubercle, 91 

Hoarseness of voice, 74 

Hospital throat v. diphtheria, 39 

Hydatid hooklets in sputum, 55 

Hyperpyrexia, a source of, 48 

Hysteria, 276 

and laryngeal troubles, 79, 80 

micturition in, 264 

v . disseminated sclerosis, 297 

Hysterical joint, 236 

Idiopathic disease, 10 
Immunity, meaning of, 31 
Inadequacy, renal, 216 
Inco-ordination, 268 

causes of, 269 

in peripheral neuritis, 294 

knee jerk in, 311 

Incubation, meaning of, 31 

period, table of, 33 

Indigestion and uraemia, 216 
Indiscriminate lesions of cord, 290 
Infection, date of, 31 

v, contagion, 24 

Inflammation as process of disease, 14 

in the lung, 85 

in nervous system, 270 

nature of irritant in, 87 

phases of, 86 



Inflammation, reparative side of, 16 
Influenza, diagnosis of, 44 

v. scarlet fever, 45 

Inhibition and interference, 267 
Inspection of chest, 65 
Interference and inhibition, 267 
Intestine, ulcers of, as cause of haemor- 
rhage, 156 
Intrathoracic tumours, 105 
Irregularity of heart, 124 
Irritant, nature of, as influencing in- 
flammation, 87 
Irritation of nerves, stages in, 315 
Irritative lesions v. destructive, 315 

Jaundice and artificial light, 167 
Joint, Charcot's, 240 

gout in, 238 

grating in, 231 

heat in, 233 

hysterical, 236 



pam in, 230 
osteoarthritis 



rheumatic gout, 



239 
Joint, redness in, 233 

rheumatism in, 238 

stiffness in, 230 

swelling of, 231 

traumatism of, 236 

tubercle of, 232, 237 

uric acid in, 240 

Joints, affections of, 229 

affections of, family history in, 234 

affections of, personal history in, 

234 
Joints, affections of, differential diagnosis 

of, 241, 243 
Joints, affections of, eburnation in, 240 
affections of, weather influence on, 

243 

Keloid, explanation of, 86 

Kidney, cirrhotic, eye changes in, 324 

cirrhotic, pathology of, 23 

conditions causing secondary 

changes in, 222 

Kidney disease and epistaxis, 150 

disease, forms of, 218 

Kidney, stone in, v. tubercle or carci- 
noma, 224 

Kidney, surgical, 197 

tubercle of, 226 

Kidneys, casts from, 206 

effect of heart failure on, 119 

haemorrhage from, 205 

latent disease of, 223 



348 



DIFFERENTIAL DIAGNOSIS 



Kidneys, malignant disease of, 227 
— — pus from, 202 
Knee jerk, 279 

as test of locality of inco-ordina- 

tion, 311 
Knee jerk in hysteria, 261 

modifications of, 260 

occasionally absent in health, 261 

Lactation, prolonged, and salicylates, 241 
Laryngeal paralysis, 76 

— trouble, blood-spitting in, 54 

recurrent, pressure on, 60 

Laryngitis, cough in, 50 
Larynx in hysteria, 79 

necessity of laryngoscope, 74 

symptoms of disease of, 74 

tumours of, 51 

ulcers of, 75 

Lead poisoning, eye changes in, 325 
— — peripheral neuritis in, 283 
Lesions, indiscriminate, of cord, 290 

irritative v. destructive, 290 

Leucocythasmia, eye changes in, 324 

epistaxis in, 149 

Levels in the nervous system, 257 
Limbs, effects of heart failure on, 119 
Liver, cirrhosis of, 180 

cirrhosis as cause of epistaxis, 150 

diagnosis of pain from, 171 

effects of heart failure on, 119 

painful affections of, 162 

Lumbago v. poliomyelitis, 293 
Lunacy in urgency cases, 336 
Lung, abscess, fcetor of, 56 

— cavity in, signs of, 84 

changes in, in pleural effusion, 105 

collapse of, 99 

consumption of, 200 

disease and haemoptysis, 153 

effects of heart failure on, 118 

gangrene of, fcetor of, 56 

inflammation in, 85, 88 

malignant disease of, 55 

tissue, in sputum, 55 

Lymphatics, pressure on, in chest, 59 

Manias, meaning of, 276 
Measles, spots in mouth in, 41 

v. rotheln, 40 

Medulla, affections of, 298 

anatomy of, 301 

physiology of, 301 

Melaena, causes of, 156 
Meninges, tumour of, 291 
Meningitis and cranial nerves, 321 



Meningitis, of cord, 290 

v. gastritis, 160 

v. myelitis, 316 

v. pneumonia, 96 

poliomyelitis, 293 

Menstruation, vicarious, and epistaxis, 

150 
Menstruation, vicarious, and haemate- 

mesis, 154 
Mental changes, functional v. organic, 278 

in brain disease, 312 

Mercurialism, tremors of, 311 
Mesentery, embolus of artery in, 161 
Microbes and disease, 27 

classification of, 26 

in sputum, 55 

proofs of specificity of, 26 

reasons for suspecting, 29 

rules governing, 25 

Micturition, increased frequency of, 188 

pathological variations of, 263 

reflex, 264 

v. defalcation, 265 

Mind, influence of, on urination, 187 

seat of, 307 

Monarthritis, 234 

Morbus cordis, haemoptysis in, 54 

pain in, 6 1 

prognosis in, 145 

Motions, examination of, 175 
Mouth, froth at, 334 

haemorrhage from, 151 

Movements, central representation of, 

257 
Movements, course of nerve impulses in, 

256 
Movements, inco-ordination of, 268 
Mucus in sputum, 53 

in urine, 192 

Murmurs, and sounds mistaken for them, 

126 
Muscles not represented centrally, 257 

reaction of, degeneration in, 269 

symmetrically used, 311 

Myelitis, acute, 291 
micturition in, 264 

Neoplasms, how they kill, 18 

and septicaemia, 20 

physiology of, 19 

and disease, 18 

Nephritis, dangers of, 219 

forms of, 218 

Nephrolithiasis, 225 

pathology of, 209 

Nerve cells, primary affections of, 320 



INDEX 



349 



Nerve diseases, central v. peripheral, 279 

diseases, differential diagnosis of, 

272 

diseases, direct v. indirect symp- 
toms, 267 

Nerve diseases, organic v. functional, 275 

diseases, primary v. reflex, 273 

impulses, motor, course of, 256 

Nerves, cranial, 303, 304, 305 

cranial, like motor spinal, 320 

cranial, lesions of, 303 

cranial, peripheral v. central lesions, 

321 

Nerves, irritation of, stages in, 315 

peripheral, functions of, 253 

thoracic, pressure on, 60 

Nervous system, anatomy of, 247 

and urgency cases, 331 

causes of disease in, 270 

diseases of, 247 

functions of, 252 

levels in, 257 

onset of diseases in, 272 

physiology of, 247 

Neuralgia, 276 

v. neuritis, 284 

Neurasthenia, 276 

Neuritis, diphtheritic, v. infantile par- 
alysis, 295 

Neuritis, inco-ordination in, 269 

in occupation neuroses, 314 

optic, 324 

optic, and vision, 324 

peripheral, 281 

peripheral, forms of, 282 

peripheral, v. amyotrophic lateral 

sclerosis, 296 

Neuritis, peripheral, v. ataxic para- 
plegia, 295 

Neuritis, peripheral, v. disseminated 
sclerosis, 296 

Neuritis, peripheral, v. lateral sclerosis, 
296 

Neuritis, peripheral, v. neuralgia, 284 

Neuritis, peripheral, v. progressive mus- 
cular atrophy, 293 

Neuritis, peripheral, v. system lesions 
of cord, 292 

Neuritis, peripheral, v. tabes dorsalis, 
294 

Neuron, the, 247 

the, functions of, 252 

Neuroses, occupation, 312 

Night, cough worse in, 52 

sweating in abscess of liver, 171 

Nomenclature of chest sounds, 74 



Nose, bleeding from, causes of, 149 
Nummulation of sputum, 54 
Nystagmus, 297 

Obstruction of bowels, 172 
Occipital lobes, function of, 307 
Occupation neuroses, 276, 312 
Oculo-motor nerves, 304 
(Edema of chest, 66, 108 
(Esophagus, pressure on, 59 
Olfactory nerves, lesions of, 303 
Operation in uraemia, 216 
Optic nerves, lesions of, 303 

neuritis, 324 

Organic v. functional nerve lesions, 275 
Osier, Dr., on bronchopneumonia, 98 
Osteoarthritis, 239 

lipping of bone in, 232 

Oxalates in urine, 208 

Pain, from old adhesions, 63 

gastric v. cardiac, 62 

girdle, 288 

in abdomen, vide Colic 

in bone, features of, 60 

in chest, 61 

in gastric ulcer, 182 

in heart disease, 113 

in joints, 230 

Palpation of chest, 66 
Palpitation in heart disease, 114 
Pancreas, painful affections of, 162 
Paradoxical anaesthesia, 282 
Paralysis, acute bulbar, 321 

after Jacksonian epilepsy, 310 

agitans, 310 

infantile, discussion of, 292 

infantile, v. diphtheria, 295 

infantile, v. exanthemata, 294 

in urgency cases, 340 

laryngeal, 76 

organic v. functional, 277 

peripheral, v. central causes of, 321 

Paraplegia, ataxic, v. peripheral neuritis, 

295 
Paraplegia in meningitis, 316 
Parasites and pyrexia, 9 

as causes of disease, 8 

Parturition, disturbances of micturition 

in, 263 
Pathogenic microbes, classification of, 

28 
Pathology, definition of, 1, 22 
Peduncles of brain, affections of, 298 
Percussion of chest, 67 
Pericardio-pleural friction, 73 



35< 



DIFFERENTIAL DIAGNOSIS 



Pericarditis, and uraemia, 216 

pain in, 61 

Pericardium, diseases of, 112 
Perihepatitis, 180 
Peritoneum, cancer of, 180 

tubercle of, 180 

Peritonitis and uraemia, 216 
Phagocytosis, definition of, 29 
Phosphates, triple, meaning of, 209 
Phosphatic diabetes, 227 
Phosphorus, forms of, in urine, 208 
Phthisis, 84 

ab luzmoptoe, 90 

after pneumonia, 94 

and chronic bronchitis, 94 

blood-spitting in, 54 

catarrhal, 89 

cough in, 51 

definition of, 85 

diarrhoea in, 94, 177 

fibroid, 89 

fibroid and keloid, 89 

from cold and cough, 92 

hsemorrhagic, 89 

pneumonic, 88 

scrofulous, 88 

tuberculo-pneumonic, 88 

Physical signs, definition of, 21 

give physical conditions only, 65 

of thoracic disease, 64 

Piles, 176 

" Pins and needles," 282 

Pleura, air or gas in, 81 

air or gas in, origin of, 80 

effect of heart failure on, 119 

effusion into, causes of, 102 

effusion into, nature of, 103 

effusion into, symptoms of, 102 

Pleurisy, acute, causes of, 10 1 

acute, pain in, 61 

acute, symptoms of, 101 

and pleural effusion, 101 

and tubercle, 101 

and uraemia, 216 

in chronic bronchitis, 100 

v. empyema, pyrexia in, 48 

Pleuro-pericardial friction, 73 
Plumbism, eye changes in, 325 
Pneumonia and phthisis, 94 

and uraemia, 216 

central, 96 

cough in, 50 

diagnosis of, 95 

hremoptysis in, 54 

is it a specific disease? 96 

■ v. intracranial inflammation, 96 



Pneumothorax, 80 

physical signs of, 82 

postulates for, 81 

sequelae of, 83 

shortness of breath in, 82 

symptoms of, 81 

Poisoning, pupils in, 333 

Poisons as cause of disease, 9 

Poliomyelitis, diagnosis of, 292 

Polyarthritis, 234 

Polypi, rectal, 176 

Pons, affections of, 298 

Portal fissure, obstruction in, 180 

Posterior longitudinal bundle, 300, 304 

Pregnancy and epistaxis, 150 

and heart disease, 147 

Pressure, intrathoracic, 59, 60 
Processes of disease, general, 13 
Prognosis in heart disease, 145 
Progressive muscular atrophy, 293 
Prostate, enlarged, micturition in, 264 
Pseudo-paralysis, 274 

Ptomaine poisoning v. cholera, 43 

Puberty and epistaxis, 149 

Pulse, frequency of, in morbus cordis, 124 

respiration ratio in pyrexia, 35 

the, in urgency cases, 335, 340 

Pupils, the, in alcoholism, 340 

the, in epilepsy, 333 

the, in fits, 333 

the, phases of, 339, 340 

the, in urgency cases, 338 

the, stupor v. coma, 339 

Purpura and epistaxis, 149 

eye changes in, 324 

Pus from bladder, 202 

in nephrolithiasis, 224 

in sputum, 53 

in urine, 200 

Pyrexia and parasites, 9 

in old thoracic disease, 49 

in phthisis, 94 

in pleurisy v. empyema, 48 

in thoracic diseases, 47 

pulse-respiration, ratio in, 35 

quickens respiration, 57 

symptoms of, 35 

Pyuria, 200 

causes of, 201 

Rales, definition of, 71 
Rashes of zymotics, table of, 37 
Reaction of degeneration, 269 
Rectum, ballooning of, 176 

diseases of, 176 

hasmorrhage from, 157 



INDEX 



35i 



Rectum v. bladder, 265 
Redness of joints, 233 
Reflexes, paths of, 259 

■ superficial v. deep, 259 

varieties of, 253 

vasomotor, 265 

Refraction, eye changes in, 325 
Renal inadequacy, 216 
Repair, limits of, in nerve tissues, 276 
Resiliency of chest wall, 68 
Respiration, accelerated, 56 

accelerated, in anaemia, 57 

accelerated, in chronic disease, 57 

accelerated, in heart disease, 57 

cogwheel, 72 

in coma, 340 

in laryngeal paralysis, 77 

ratio to pulse in pyrexia, 35 

rhythm, alterations in, 49 

Retention of urine, causes of, 217 

v. suppression, 216 

Rheumatic gout, 238 

Rheumatism, cases where salicylates are 

no use, 241 
Rheumatism, gonorrhoeal, 235 

joints in, 238 

peripheral neuritis in, 283 

simple v. gonorrhoeal, 236 

v. rheumatoid arthritis, 242 

Rheumatoid arthritis, 239 

v. rheumatism, 242 

Rhonchus, definition of, 71 

Rigors v. convulsions, 95 

Root symptoms, 288 

Rotheln v. measles and scarlet fever, 40 

Salicylates, occasionally no use in rheu- 
matism, 241 

Salt as detector of gastric ulcer, 183 

Scar tissue, functions of, 16 

Scarlet fever v. influenza, 45 

v. measles, 40 

v. rotheln, 40 

Scarring in varicella, 38 

Schott treatment of morbus cordis, 146 

Sciatica from pressure, 274 

v. neuritis, 284 

■ v. poliomyelitis, 293 

Sclerosis, amyotrophic, v. peripheral 
neuritis, 296 

Sclerosis, disseminated, v. functional 
trouble, 297 

Sclerosis, disseminated, v. peripheral 
neuritis, 296 

Sclerosis, early stages of, v. functional 
trouble, 322 



Sclerosis, lateral, v. peripheral neuritis, 

296 
Sclerosis, primary, of nerve cells, 320 

secondary, 320 

Segregation, necessity for, 33 
Sensation, cortical seat of, 307 

pathways of, 257 

Septicaemia, 28 

from neoplasms, 20 

Serum-therapy, arguments for, 5 
Shock and alcoholism, 329 

nature of, 313 

Shortness of breath v. dyspnoea, 58 

Sight, cortical seat of, 307 

Signs, physical, of thoracic disease, 64 

physical, v. symptoms, 21 

Sixth cranial nerve, localisation from, 

302, 304 
Smell, cortical representation of, 307 
Sodium phosphate in urine, 208 
Spasm, organic v. functional, 277 
Speech in laryngeal paralysis, 77 

anatomy of, 249 

Spinal cord, functions of, 255 

diseases of, 285 

Spleen, heart, 119 

painful affections of, 162 

Sputum, the, as aid to diagnosis, 52 

blood in, 54 

foetid, v. foul breath, 56 

fcetor of, 55 

in pneumonia, 96 

nummulation of, 54 

qualitative changes in, 53 

quantity of, 53 

Squint, inco-ordination in, 269 
Stiffness of joints, 230 
Stomach, effects of heart failure on, 119 
Stone in kidney, 202, 225 

v. carcinoma, 224 

v. tubercle, 224 

Strangury, micturition in, 265 

definition of, 204 

Structure in disease, 14 

Succussion, 73 

Sugar in urine, 212 

Suppression v. retention of urine, 216 

causes of, 217 

Supramarginal lobes, functions of, 307 
Surgical kidney, 197 
Sweat, the, in urgency cases, 334 
Sweating at night, 171 

in empyema, 48 

Swelling in joints, 231 
Symptomatology, definition of, 22 
Symptoms, definition of, 21 



352 



DIFFERENTIAL DIAGNOSIS 



Symptoms, direct v. indirect, in nerve, 

267 
Symptoms, root, 288 

v. physical signs, 21 

Synovitis, 237 
Syphilis of cord, 290 

v. septic venereal trouble, 46 

v. variola, 38 

Systems in spinal cord, 287 

lesions of, v. peripheral neuritis, 

292 

Tabes dorsalis, micturition in, 263, 265 

v. peripheral neuritis, 294 

Tactile vocal fremitus, 66 
Tegmentum crura cerebri, 308 
Temperature in bronchitis, 98 

in bronchopneumonia, 98 

in capillary bronchitis, 48 

in coma, 341 

in hemiplegia, 319 

in urgency cases, 337 

Thalamus, optic, 308 
Thorax, pressure effects in, 59 

symptoms of disease in, 47 

tumours of, 105 

Throat, hospital, v. diphtheria, 39 
Tinkling sounds, 72 
Tissue debility as cause of disease, 12 
Tongue, the, functions of, 305 
Toxaemia, functions of body cells in, 16 

nervous phenomena in, 276 

Tracheal affections, blood-spitting in, 54 

tugging, 109 

Tracts in cord, functions of, 288, 289 

motor, 256 

sensory, 257 

Traumatism and degeneration, 313 

and tumours, 313 

as cause of disease, 8 

as urgency case, 328 

of joints, 236 

of nervous system, 290, 312 

Tremors, functional v. organic, 297 
Triple phosphates, meaning of, 209 
Trophic influences of nerves, 254, 266 
Trousseau on hemiplegia, 319 
Tubercle and age, 238 

and bronchopneumonia, 100 

and pleurisy, 101 

and tubercular v. nodule and no- 
dular, 90 
Tubercle, cough in, 50 

heredity in, 91 

in choroid, 325 

in joints, 237 



Tubercle in kidney, 202, 226 

in kidney v. stone or carcinoma, 

224 
Tubercle, miliary, 90 

pulmonary, diagnosis of, 90 

v. bronchitis, 91 

v. bronchopneumonia, 91 

v. ulcerative endocarditis, 145 

Tugging, tracheal, 109 
Tumour bulging from chest, 66 

of thorax, 105 

of brain and cord, 322 

and cranial nerves, 321 

eye changes in, 325 

haemorrhage into, 315 

headache in, 323 

vomiting in, 323 

Typhoid, eye changes in, 324 

state, the, 42 

v. typhus, 41 

v. ulcerative endocarditis, 144 

Ulcer, duodenal, as cause of melasna, 

156 
Ulcer, gastric, and haematemesis, 155 

gastric, salt as detector of, 183'" 

gastric, v. dyspepsia, 182 

of larynx, 75 

of nose as cause of epistaxis, 149 

Ulcerative endocarditis, 141 
Unconsciousness in urgency cases, 337 
Uraemia, 214 

as cause of vomiting, 159 

as urgency case, 333 

diagnosis of, 215 

pupils in, 334 

v. haemorrhage as cause of coma, 

34i 
Urates in urine, 192, 207 
Urea and uric acid, 210 
Ureter, blocking of, by tubercle, 226 

blocking of, by stone, 225 

Urgency cases, 326 

diagnosis of, 332 

Uric acid, 209 

in joints, 240 

Urinary organs, diseases of, 185 
Urine, the, acidity of, 186 

blood in, 203 

bile in, 190 

casts in, 205 

characters of healthy, 185 

colour of, 189 

deposit in, 192, 194 

incontinence of, 264 

in disease, 188 



INDEX 



353 



Urine, in urgency cases, 340 

in Bright' s disease, 221 

oxalates in, 208 

pathology of, 190 

phosphates in, 208 

pus in, 200 

quantity of, 188, 189 

specific gravity of, 190 

sugar in, 212 

suppression of, 216 

urates in, 207 

variations in health, 186 

Uvula, elongated, causing cough, 50 

Varicella, scarring in, 38 

v. variola, 38 

Variola v. poliomyelitis, 292 

v. syphilis, 38 

v. varicella, 38 

Vasomotor reflexes, 254, 265 
Veins, enlarged, on chest, 66 

pressure on, in thorax, 59 

Venereal infection, differential diagnosis 
of, 45 



Venereal infection, septic v. syphilitic, 

46 
Vessels, lesions of, in urgency cases, 328 
Vision, and optic neuritis, 324 

as cause of inco-ordination, 269 

double, 304 

Voice, hoarseness of, 74 

sounds, 71 

Vomica, signs of, 84 
Vomiting, 158 

causes of, 159 

in cerebral tumours, 323 

in colic, 165 

nervous, 159 

Watson, Sir T. , on haemoptysis, 93 
Wear and tear as causes of disease, n 
Weather, the, and joint trouble, 243 
the, influence of, on urine, 187 

Zymotics as cause of vomiting, 159 

diagnosis of, 30 

rashes in, 37 



DEFECTIVE EYESIGHT: 

The Principles of Its Relief by Glasses. 



D. B. ST. JOHN ROOSA, M.D., LL.D., 

Professor Emeritus of Diseases of the Eye and Ear; Post-Graduate Medical 

School and Hospital ; Surgeon to the Manhattan Eye and Ear Hospital, 

etc., etc.; author of "A Clinical Manual of Diseases of the Eye" ; 

"Ophthalmic and Otic Memoranda " ; "A Practical Treatise 

on the Diseases of the Ear"; "The Old Hospital and Other 

Papers"; "A Vest-Pocket Medical Lexicon." 



Cloth. i6mo. $1.00, net. 



Dr. St. John Roosa has revised and very carefully enlarged the first edi- 
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quiring the use of glasses, and indicates in the most careful manner the 
indications and rules for describing them. It contains six chapters, and 
is illustrated, so that a perfect understanding of the text is made easy. It is 
well known that the author is aconservative in regard to the value of glasses, 
believing that there is a limitation to their use, and that they ought not to 
be prescribed unless of positive value. The revolution which has been pro- 
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exact instrument for measuring the radius of the cornea, is fully dwelt upon. 
No pains have been spared to make the manual a complete guide to the 
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one which concerns such a large proportion of the human race. 



THE MACMILLAN COMPANY, 

66 FIFTH AVENUE, NEW YORK. 

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A Brief but Comprehensive Text- A Handy Book of Reference for 

Book for the Student. the Skilled Physician. 

KLEMPERER'S 
CLINICAL DIAGNOSIS. 



DR. G. KLEHPERER, 

Professor at the University of Berlin. 

Second American from the seventh and last German edition ; au- 
thorized translation by Nathan E. Brill, A.M., M.D., Adjunct 
Attending Physician, Mt. Sinai Hospital, and Samuel M. 
Brickner, A.M., M.D., Assistant Gynaecologist, Mt. Sinai 
Hospital Dispensary. With 61 Illustrations. 



Cloth. i2mo. Price, $1.00, net. 



" Those of us who have heretofore made the acquaintance 
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it has so long enjoyed." — N. Y. Medical Journal. 



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